tag:blogger.com,1999:blog-14433450823983725352024-03-05T15:30:15.134-07:00In VivoSkepticism and science for all!C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.comBlogger188125tag:blogger.com,1999:blog-1443345082398372535.post-34756585694029471232012-10-08T10:01:00.000-06:002012-10-08T10:01:50.696-06:00And the 2012 Nobel Prize in Medicine or Physiology goes to.......Sir John B. Gurdon and Shinya Yamanaka for the discovery that mature cells can be reprogrammed to become pluripotent.<br />
<br />
Gurdon's major work in this area goes back to the 1960s. In '62, in what would become a classic experiment in developmental genetics, he removed the nucleus from a <i>Xenopus</i> egg cell, replacing it with the mature nucleus from an intestinal cell<sup>1</sup>. This modified egg cell then developed into a fully normal tadpole, indicating that the intestinal cell, despite being fully differentated, still held all the necessary 'instrictions' to form an entire organism. This became one of the pioneering experiments in both developmental genetics and nuclear transplantation. Gurdon's work was perhaps most important because it challenged the then prevalent dogma that a cell's fate was set in stone once it became specialized. Gurdon showd that this was not the case.<br />
<br />
Yamanaka's major contribution is much more recent. Yamanaka was studying embryonic stem cells, which are always in an immature, undifferentiated state. He was interested in identifying the genes which kept these cells immature, and after finding and identifying a number of them, he wondered whether these genes could be used in mature cells to induce them to revert back into pluripotent stem cells<sup>2</sup>. He and his team introduced four of the identified genes into mature fibroblasts, and observed that the mature cells would revert back into stem cells. These induced pluripotent stem cells (iPSC) could then go on to differentiate into many other cell types. This was a major breakthrough, and the discovery was lauded in all corners of the scientific world. <br />
<br />
Both these discoveries have lead to research in medicine that could change the world, and many of the potential applications have yet to be realized. The use of iPS cells in effectively treating diseases or correcting genetic disorders is just on the horizon. Both the pioneering work of Gurdon and the breakthrough work of Yamanaka are definitely worthy of the Nobel Prize, indeed!<br />
<br />
---------------------------------------<br />
<br />
1. <span class="reference-text"><span class="citation Journal"><strong class="selflink">Gurdon, J. B.</strong>;
Elsdale, T. R.; Fischberg, M. (1958). "Sexually Mature Individuals of
Xenopus laevis from the Transplantation of Single Somatic Nuclei". <i>Nature</i> <b>182</b> (4627): 64–65</span></span><br />
<span class="reference-text"><span class="citation Journal">(Read it <a href="http://dev.biologists.org/content/10/4/622.long">here</a>!) </span></span><br />
<span class="reference-text"><span class="citation Journal"><br /></span></span>
<span class="reference-text"><span class="citation Journal">2. T<span class="reference-text"><span class="citation Journal">akahashi, K.; <strong class="selflink">Yamanaka, S.</strong> (2006). "Induction of Pluripotent Stem Cells from Mouse Embryonic and Adult Fibroblast Cultures by Defined Factors". <i>Cell</i> <b>126</b> (4): 663</span></span></span></span>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-68174884824906363652012-10-07T09:44:00.001-06:002012-10-07T09:44:36.469-06:00The Obligatory 2012 pre-Nobel Prize PostIt's that time of year again! The 2012 Nobel Prizes will be handed out this week. Oct. 8th will be the first, in Physiology or Medicine. Physics is on the 9th, Chemistry on the 10th. The Peace, Economics and Literature prizes are to follow but who cares about those, really?<br />
<br />
Any predictions on the winners? You can find a list of predicted winners by David Pendleburry, who has in the past made a number of accurate predictions, <a href="http://sciencewatch.com/nobel/2012-predictions">here</a>. I have no predictions myself, this year, so the winners will be a surprise for me.<br />
<br />
As usual, I'll post the winners on my blog as they happen.C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-37449627297009859762012-08-09T17:01:00.000-06:002012-08-09T17:01:40.803-06:00Yet Another Daily Dose of Science Journalism FailFrom the Daily Mail's website (where else) <a href="http://www.dailymail.co.uk/health/article-2185597/Babies-born-naturally-higher-IQs-delivered-caesarean-section.html">comes the following headline</a>:<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi7AqUSy917x_ejaKPejuS9ZN6zu7c9_sdTB5aaPZjMItSK0ktBoWTDIBB8Tzm8nNuCsRX31-1rKhPw6I1t7aMZ9dZXunANoc4XE2q1_zpVRjimgXln_rfrxhdkXFsAzDgNGLwXY4uSjMQ/s1600/DailyMailFail.PNG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="201" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi7AqUSy917x_ejaKPejuS9ZN6zu7c9_sdTB5aaPZjMItSK0ktBoWTDIBB8Tzm8nNuCsRX31-1rKhPw6I1t7aMZ9dZXunANoc4XE2q1_zpVRjimgXln_rfrxhdkXFsAzDgNGLwXY4uSjMQ/s640/DailyMailFail.PNG" width="640" /></a></div>
<br />
That's a pretty weighty claim. Do babies born via C-section really have lower IQs than those born naturally? What does the article go on to say?<br />
<blockquote class="tr_bq">
<span style="font-size: small;">"</span><span style="font-size: small;">According to scientists, when women
give birth naturally there are higher levels of a special protein in
babies’ brains that helps boost intelligence levels as they develop.</span><br />
<span style="font-size: small;">Scientists
at Yale University in the US say the increased levels of the protein,
called UCP2, in babies born naturally could help foster their short and
long term memories – key components of the human IQ – as they grow up."</span></blockquote>
So according to the Daily Mail, babies born naturally have higher levels of UCP2 in their brains, and this means they have higher IQs. And, as is always the case, the Daily Mail has failed to cite the actual research behind their claim. So, I went ahead and <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042911">found it</a> for myself<sup>1</sup>. What do the original authors have to say?<br />
<br />
From their abstract (emphasis added):<br />
<blockquote class="tr_bq">
"Mitochondrial uncoupling protein 2 (UCP2) is induced by cellular stress
and is involved in regulation of fuel utilization, mitochondrial
bioenergetics, cell proliferation, neuroprotection and synaptogenesis in
the adult brain. Here we show that natural birth in <b>mice</b> triggers UCP2
expression in hippocampal neurons."</blockquote>
And from their discussion (again, emphasis added):<br />
<blockquote class="tr_bq">
"The current data suggests that the induction of <em>Ucp2</em> by birth
-associated physiological stress <b>enables metabolic adaptation to a
switch available nutrient utilization that is critical for proper
survival and development of hippocampal and other brain neurons</b>."</blockquote>
So, in other words, 1) the study was done in mice, and 2) UCP2 levels are correlated with changes in metabolism that were important for brain growth. Nowhere in the paper do the authors mention human babies and nowhere do they mention UCP2 levels having any effect on IQs. One has to wonder whether Sarah Johnson at the Daily Mail actually read the original paper.<br />
<br />
Then again, <a href="http://botanybugsandbunkum.blogspot.ca/2012/01/ants-atavisms-and-journalism.html">the Daily Mail never really has been good at that science thing</a>. They don't call it the Daily Fail for nothing.<br />
<br />
----------------------------------------------- <br />
<span class="citation_author">1. Simon-Areces
J,
</span>
<span class="citation_author">Dietrich
MO,
</span>
<span class="citation_author">Hermes
G,
</span>
<span class="citation_author">Garcia-Segura
LM,
</span>
<span class="citation_author">Arevalo
M-A,
</span>
<span class="citation_author">et al. </span>
<span class="citation_date">(2012)</span>
<span class="citation_article_title">Ucp2 Induced by Natural Birth Regulates Neuronal Differentiation of the Hippocampus and Related Adult Behavior.</span>
<span class="citation_journal_title">PLoS ONE</span><span class="citation_issue"> 7(8):</span>
<span class="citation_start_page">e42911.</span>
<span class="citation_doi">doi:10.1371/journal.pone.0042911</span> <br />
<br />
<span class="citation_doi"></span><div class="intro">
</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-63262661727590358052012-08-08T01:49:00.002-06:002012-08-08T01:49:55.736-06:00A Few Little ChangesThough nothing drastic. I've made some changes to the Blogroll on the right. I removed a couple of blogs which are no longer active, and I also added a few new blogs which I think are pretty interesting. If you see one you're not familiar with, do check it out!C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-20352967471318640932012-07-02T22:45:00.001-06:002012-07-02T22:47:07.628-06:00Addition of Genetic Information Redux: A Critical Response to a Critical Response<span xmlns=""></span><br />
<span xmlns="">A few years ago ( when my blog was a bit more active than it is today) <a href="http://cwgk.blogspot.ca/2009/01/addition-of-genetic-information-made.html">I wrote up a post rebutting</a> the old creationist canard that evolution requires "new" genetic "information" to be added to a genome, and, furthermore, that such a process is impossible and consequently, evolution is false. Recently, a LiveJournal user by the name of <a href="http://jair-greycoat.livejournal.com/">Jair_greycoat</a> wrote up a <a href="http://jair-greycoat.livejournal.com/770.html">response</a> to my article. After reading it, I think that there are a number of points that I should clarify and some misconceptions that should be corrected. Such a task is too much for the LiveJournal comment section, so I've written up my reply to the criticisms below.</span><br />
<br />
<span xmlns="">"<b>Why would creationists claim that beneficial mutations are rare or impossible? Didn't the author of the above quote just provide a real, observable example? The only claim I have heard from creationists regarding this is that all, or nearly all, such beneficial mutations are a result of a loss in information, not a gain. I have not personally heard them claim that the loss of information cannot be helpful. We do have a saying, "ignorance is bliss." If a person's body is "ignorant" of alcohol, then they have "bliss"--they can't get drunk, or so I've heard. Nevertheless, the author of the quote agrees with the creationists that the mutation is a loss of information</b>."</span><br />
<br />
<span xmlns="">Why would Creationists claim such a thing? Your guess is as good as mine. The scientific literature is replete with examples of mutations which confer a beneficial or improved phenotype. The classic example of sickle-cell anaemia is one, as is lactase persistence in European populations (see <a href="http://evolution.berkeley.edu/evolibrary/news/070401_lactose">here</a> and <a href="http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1000491">here</a>). Creationists, nonetheless, are not always ones to let reality get in the way of their religious beliefs, and routinely claim that beneficial mutations do not – and cannot – occur. The argument is quite common in the Creationist literature; see <a href="http://www.creationstudies.org/operationsalt/myth-beneficial-mutations.html">this article</a> from Creationstudies.org for example, "<i>The Myth of Beneficial Mutations</i>", which outright claims "The bottom line is that mutations always weaken an organism". Other examples of this can be seen <a href="http://www.trueorigin.org/mutations01.asp">here</a> and <a href="http://www.youtube.com/watch?v=WrUy5GUJxeg">here</a> and <a href="http://www.metacafe.com/watch/4036816/no_beneficial_mutations_not_by_chance_evolution_theory_in_crisis/">here</a>. The claim comes up so often that even <a href="http://www.answersingenesis.org/articles/aid/v4/n1/beneficial-mutations-in-bacteria">Answers in Genesis had to tell people to stop using it</a>.</span><br />
<br />
<span xmlns="">The claim that beneficial mutations only come about by a loss of information, as you mention, is another claim that comes up - one that is equally false. The example of sickle-cell anaemia as mentioned above is not due to a "loss of information" (which I take as to mean a deletion in a gene) but rather due to a change in a single nucleotide in the gene – from an A to a T. This change results in a protein that is altered in one amino acid, and confers resistance to malaria. Another example is the <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC349650/?tool=pubmed">evolution of lactulose metabolism in <i>E.coli</i></a>, which occurred not through the "loss of information" but rather from a genetic recombination within a previously existing gene; that is to say, the "information" (for the lack of a better term) was rearranged and gave rise to a novel, beneficial function. Or how about <a href="http://www.pnas.org/content/106/29/11827.full">this interesting example</a>: some placental function in vertebrates is due to a proviral gene that is integrated into our genome – again, a gain of genetic "information", rather than a loss of it. The point I'm trying to make is that for every example you can point to where a beneficial phenotype has arisen due to a genetic deletion, you can also point to one that was caused by a gain of "information".</span><br />
<span xmlns=""> </span><br />
<span xmlns="">It is one facet of this "gain of information", namely diversification of gene function via genetic duplications, that the rest of my article aimed to address. The creationist claim I was rebutting was that a "gain of genetic information" is impossible, and I went on to provide a mechanism whereby it can occur.</span><br />
<br />
<span xmlns="">"<b>The</b><b> author then says that the term "information" is too vague and not defined by creationists. Personally I've never had a problem with the word, I think it means exactly what it sounds like it means.</b>"</span><br />
<br />
<span xmlns="">Perhaps he does not realize that the word "information" has multiple specific meanings in science. When a creationist mentions "information", are they meaning actually physical information? In which case, are they referring to classical information or quantum information? Or maybe they mean information in the technological sense, as in "instructions" or "code"? A loss or gain of "information" takes on very different meanings depending on which sense of the word you're using. "Information" is a rather clumsy word to use when describing genetics for this reason, and it is not used widely in the biological community. Its use in reference to genetics seems to be restricted to Creationists.</span><br />
<br />
<span xmlns="">"<b>Why would creationists claim that genes are never added to a genome? Of course genes are added; I think we can agree on that. What I have heard creationists deny is that these new genes contain new and original content, or that they are capable of transforming into new and original content that is not simply random garble.</b>"</span><br />
<br />
<span xmlns="">See above. Creationists claim that because they are either ignorant of the facts or refuse to accept them.</span><br />
<br />
<span xmlns="">"<b>Now I realize that the writer is probably using the words "gene" and "information" interchangeably</b>."</span><br />
<br />
<span xmlns="">Again, refer to my explanation of the problems with using the word "information" above. I used "information" throughout my original article because it is the term that Creationists throw around all the time. I use it in quotes to show that it is an ill-fitting word be using in such a context. I used "information" to refer to both genes and gene sequences, since that is what I think Creationists mean when they throw the term around.</span><br />
<br />
<span xmlns=""><b>"Then the author goes on to quote Ross Hardison. As I see it, the quote is essentially a hypothesis about the evolution of a haemoglobin gene. I don't have any questions about it except this part: "In this way, the two genes that started out identical acquired sequence differences and later, functional differences." But how do these mutations become functional differences rather than just causing everything to fall apart, as I would expect from entropy?</b>"</span><br />
<br />
<span xmlns="">To answer this, you must really think about just what a mutation means to the gene it's situated in. A mutation, whether it is a deletion, addition or just a change in the sequence, carries with it the risk of altering the sequence of the protein for which it codes. Proteins get their function from their shape, and their shape is directly (more or less) determined by their amino acid sequence. As mutations accumulate in a duplicated gene, the chance of these mutations altering the function of the protein it encodes rises. Of course, it is not guaranteed that these alterations will be of any benefit, but that's where natural selection plays a role. In those instances where the mutations are harmful, the gene is less likely to be passed on. Those that confer some benefit are more likely. In this manner, over generations, the net effect becomes a positive one. When we look at the haemoglobin gene today, we're looking at it with a bias – we only see the mutations which were passed on through the generations and not the harmful ones that were weeded out. </span><br />
<br />
<span xmlns="">Have you ever played the game Yahtzee? In that game, you have to roll five dice, and you're scored based on the combination of numbers that result. The best score you can get on a turn – the eponymous Yahtzee – is to get a 6 on all five dice. The chances of getting a Yahtzee are pretty low, only 1 in 7776. But the game lets you roll the dice three times, and you're allowed to select the dice you want to keep between rolls. So if you roll 6 on two dice on your first attempt, you can keep those and only roll the remaining three on your second try. In this manner you greatly increase your chance of scoring a Yahtzee; it now becomes 1 in 22 (see <a href="http://mathforum.org/library/drmath/view/52174.html">here</a> if you're interested in the math behind it). Natural selection works in exactly the same principle. The odds of getting a beneficial new function out of random mutations is low without selection. But selection allows those good mutations to be saved and the bad ones to be discarded. Once you apply selection, novel functions can arise quickly and easily. </span><br />
<br />
<span xmlns="">I should also point out here that even a loss of function or a reduced function is still a functional <i>difference</i>. Any mutation that is not neutral or silent, by definition, results in some functional difference. The question, then, should not be "how do mutations become functional differences" but rather, "how do these mutations result in something that is beneficial rather than deleterious", the answer to which is natural selection.</span><br />
<br />
<span xmlns="">One other point that I would like to make before continuing is regarding the author's use of the word "entropy". I have seen this word tossed about by Creationists more times than I can count, and in almost all the cases, they are not using the word in the correct sense. Creationists are often quick to cite the Second Law of Thermodynamics as "Over time, the amount of entropy in a system increases", and then claim that evolution violates this principle as it requires that over time, entropy must <i>decrease</i>, viz. genomes becoming more ordered rather than degrading into non-coding gibberish. The Second Law of Thermodynamics is no obstacle to evolution, however, as the definition of the law cited by Creationists leaves out a pivotal point: that it applies only to a <i>closed system</i>, that is, a system where there is no flow of energy into or out of it. Biological systems are, of course quite open, with energy flowing freely into and out of them. Genomes are under no obligation to fall victim to increasing entropy. </span><br />
<br />
<span xmlns=""><b> "Again from the main article, I quote: "I can already hear the cries of the creationists. "But," they proclaim, "this doesn't show evolution at all, for the different haemoglobin genes are still all the same <i>kind</i>!" (Oh how I hate that dreaded "kind" word)." I'm going to step out and say that I have never heard any serious creation-scientist speak or write a sentence like that one. It does not even make sense in context. Why would a creationist talk about "kinds" with regard to genes in the first place? "Kinds" as far as I have heard it used, is a word used by creationists to refer to different species. It would make more sense, I think, if the sentence was written as: "But," they proclaim, "this doesn't show evolution at all, because it is only a story which doesn't explain the fundamental difficulty! How can random mutations produce meaningful structures which help a species' survival?""</b></span><br />
<span xmlns=""><b><br /></b></span><br />
<span xmlns="">I cannot comment about how familiar the author is with the claims of "serious creation-scientists" but the "kind" argument is one that I've heard a mindboggling number of times. It seems to be a favourite of Kent Hovind and Ken Ham. They argue that "no dog ever gives birth to a cat" (which, if it occurred, would be a blow <i>against</i> evolution, not in support of it) and that's because dogs are one "kind" and cats are another "kind". The major problem with the "kind" talk is that Creationists never use the word in a consistent manner. The author claims that they use "kind" synonymously with "species", which is blatantly false. Are "dogs" and "cats" species? Creationists will claim that <i>Drosophila melanogaster</i> is a "kind", but also that flies in general are a "kind". They use the word to refer to whichever biological taxon is convenient to them at the time, whether that be a species, genus, family or other taxon. It is in this sense that the hypothetical Creationist response that I proposed makes sense. The haemoglobin example I used show how new, but similar, haemoglobin genes evolved. The likes of Ham and Hovind would classify these as the same "kind" in the same way they classify dog breeds as "kind" (note that I'm not saying that such a comparison is justified, only that it is one that I imagine Creationists would make). The remainder of the paragraph the author quoted then went on to explain how new <i>different</i> functions can arise.</span><br />
<br />
<span xmlns="">"<b>The</b><b> article explains that new structures--new content in the genetic code--can come from numerous mutations over time. Bad mutations would be weeded out by natural selection, and good ones kept. This made sense to me--on the surface--collect enough mutations over enough time, and there is the possibility of hitting a combination containing survival value simply by chance. I'll try to explain why I think it doesn't make sense on a practical level later in this entry</b>."</span><br />
<br />
<span xmlns="">Here the author demonstrates that he does understand the process of natural selection, if only superficially. This makes me wonder why he seems to have difficulty understanding how this principle can be applied to duplicated genes evolving novel functions.</span><br />
<br />
<span xmlns=""><b>"I don't know exactly what percentage of mutations creationists claim are harmful. However, isn't any mutation that isn't beneficial, a potentially harmful one? Especially when you have a large number of mutations, each being by itself neutral or nearly so; but when many such mutations pile on, it doesn't matter--the overall original function of the gene is destroyed, because it no longer contains the original instructions for whatever structures it previously needed to survive...</b><b>Why would only one of the copies be mutated? Wouldn't both of them mutate at the same rate?"</b></span><br />
<span xmlns=""><b><br /></b></span><br />
<span xmlns="">As mentioned above, Creationists alternately claim that all mutations are harmful, or that most mutations are harmful. The reality is that the vast majority of mutations are neither harmful <i>nor</i> beneficial. Most mutations are neutral, that is to say, they have no affect on the gene at all. Since the genetic code is redundant (<i>i.e.</i> there are many nucleotide codons which code for any given amino acid), most mutations won't affect a protein's sequence at all. Furthermore, similar codons code for amino acids that are chemically similar, so a mutation that does alter the protein sequence will not necessarily alter the protein's function. These neutral mutations confer no advantage or disadvantage on an organism and are therefore invisible to the eyes of natural selection. If a gene were to acquire a large number of neutral mutations, it's affect on the gene would be minimal precisely because they are neutral! The original function of the gene would not be destroyed at all. </span><br />
<br />
<span xmlns="">As for mutation rates: yes, it would be safe to assume that both the genes would have the same mutation rate. However, it has little bearing on the ultimate fate of the genes. The reason we see many more mutations in one copy of the gene and not the other is because a deleterious mutation in <i>both</i> copies could prove lethal. Any organism that had both copies mutated in such a way would die and those versions of the genes would not get passed on to successive generations. However, it that same deleterious mutation occurred in one copy and not the other, this would not affect the organism since it still has an original, functional copy remaining. The other copy is free to accumulate mutations as long as there is still an original, functional copy remaining. </span><br />
<br />
<span xmlns="">"<b>But in order for a mutation to be considered helpful to a creature's survival and therefore selected by nature, doesn't it have to be part of a fully functional structure from the very start? If not, in what way is the mutation helpful? I believe that even if the mutation is comparable to the first steps in building a genetic program, until that program is finished and complete, it will be a drain on the organism's resources, and therefore harmful</b>. I<b> should think then, that even mutations that could in the future be beneficial (those that are not merely losses of information) would be weeded out by natural selection. Hence why the article I quote from does not make sense to me in this respect. "Fundamentally, this type of evolution requires natural selection to step into the picture and choose between variations--which organism is most fit. But isn't natural selection a blind process? At least according to atheists, I have heard that it is. How can a blind process select for mutations that have the future potential to be part of new functions and structures, yet have no survival value (or worse, are a net drain on the organism) in the present?</b>"</span><br />
<span xmlns=""><b><br /> </b></span><br />
<span xmlns="">What the author presents here is his own version of the Irreducible Complexity (IC) argument. "What use is half a wing?" the argument often goes. The examples that are usually brought up – the eye, the bacterial flagellum – have been debunked countless times. I could write an entire blog entry on the problems with the Irreducible Complexity argument, so forgive me for being terse here. The major flaw in IC is that it does not account for the gradual adaptation of one biological system for a different, novel function. What good is half a flagellum to a bacterium, you ask? Well, it works great as a <a href="http://en.wikipedia.org/wiki/Type_three_secretion_system">Type III Secretion system</a>. Sure, if you removed any of the flagellar components, it might cease to function as a flagellum. But that ignores the fact that the "half a flagellum" may have some other evolutionary adaptation entirely. This can be said of any supposedly "irreducibly complex" system. Interested readers can read more about the problems with the IC argument at <a href="http://www.talkorigins.org/faqs/behe.html">TalkOrigins</a>.</span><br />
<br />
<span xmlns="">"<b>If by "no new genetic info" the author means "no new and original content" rather than copies of previously existing genes, then the reason the claim is so common is because (as far as I know) there is no explanation from evolutionists as to how new and original information can come from mutations and natural selection."</b></span><br />
<span xmlns=""><b><br /></b></span><br />
<span xmlns="">If this is the case than the author has either misunderstood the mechanism that I have described in my article or is unfamiliar with the criticisms of Irreducible Complexity. Again, I refer to the TalkOrigins article I linked to above.</span><br />
<br />
<span xmlns="">"<b>What about the creation-scientists who are also part of the scientific community and who probably say quite loudly that gene duplication is not a sufficient mechanism for evolution? This quote just feels like the author of the article is intentionally ignoring them. This probably bothers me even more than the article's explanation for gene evolution, because it seems to imply that the author, at some level, does not see creation-scientists as "real scientists". That is just wrong, especially as I have seen plenty of books written by them, and those which I read made plain and simple sense to me. Certainly more sense than the article I quote from made</b>."</span><br />
<br />
<span xmlns="">The author does get this one thing correct: I don't consider "creation-scientists" to be real scientists. If the author has any particular individuals in mind who he feels are real, practicing scientists, I would love to know who they are. But for the most part, "creation scientists" fit one or more of the following descriptions:</span><br />
<ol>
<li><span xmlns="">Do not have a degree in a scientific field related to evolution (evolutionary biology, molecular biology, etc.).</span></li>
<li><span xmlns="">Do not have a degree from a recognized, accredited institution.</span></li>
<li><span xmlns="">Do not publish actual research in peer-reviewed scientific journals.</span></li>
</ol>
<span xmlns="">Unfortunately, if they do not match these criteria, then they're not real scientists. It might sound harsh but that's the way science works. Again, if the author has literature from a scientist who holds a relevant degree from an accredited institution that has been published in a peer-reviewed journal, I'm all ears. But until then, I'll give "creation scientists" all the credit they deserve; which is to say: none.</span>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-7918613412770784562012-03-05T12:06:00.000-07:002012-03-05T12:06:00.936-07:00Another Daily Dose of Science Journalism FailCare of <i>The Telegraph</i> comes <a href="http://www.telegraph.co.uk/science/evolution/9123601/Eel-like-creature-identified-as-earliest-human-ancestor.html">this sensationalist little blurb</a>:<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhTeNTSyxBhcy34KxsXFdKHbrZWwH3LNdleYuDLnPGQt53s99bvjvnGe6rv1vLZnDxj9AzK1CXjKlOqKd8YtEs18x84WV-3PgkbElw9YBjoDHI4VnX-rJ4UPVpQDq8BFqC7wClff80MAk0/s1600/journalismfail.JPG" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhTeNTSyxBhcy34KxsXFdKHbrZWwH3LNdleYuDLnPGQt53s99bvjvnGe6rv1vLZnDxj9AzK1CXjKlOqKd8YtEs18x84WV-3PgkbElw9YBjoDHI4VnX-rJ4UPVpQDq8BFqC7wClff80MAk0/s400/journalismfail.JPG" width="400" /> </a></div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: left;">If the fact that the "earliest human ancestor" is eel-like doesn't push your incredulometers into the "Something Isn't Right Here" zone, then consider this line from the article: </div><blockquote class="tr_bq">"Fossils dating back 505 million years preserve the relics of tiny, slithering animals which are the oldest life forms ever discovered with primitive spinal cords. </blockquote><div class="secondPar"> <blockquote> As the precursor of vertebrates the species is also believed to be the direct ancestor of all members of the chordate family, which includes fish, birds, reptiles, amphibians and mammals."</blockquote>Ah, well, that makes much more sense! But, that means the headline is incredibly misleading. This fossil is not simply the ancestor to humans, it's the ancestor to all chordates! That includes bats, bears, dogs, cats, aardvarks, aardwolves, all manner of fishes, frogs, salamanders, dinosaurs, eagles, parrots, rats, mice, koalas, kangaroos, bison, pigs, goats....you get the idea. Yes, Chordata does include humans, but it includes anything with vertebrae (and <a href="http://en.wikipedia.org/wiki/Cephalochordata">some</a> <a href="http://en.wikipedia.org/wiki/Tunicate">things</a> without them).Calling this the "earliest human ancestor" is yellow journalism, as far as I'm concerned. That's not to say that this finding isn't interesting. It is! But to define it in the context that the <i>The Telegraph</i> has done is misleading and sensationalist, and only further drives my conviction that science communication should be left to the scientists.<br />
</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com2tag:blogger.com,1999:blog-1443345082398372535.post-42134478169955766252012-01-19T22:39:00.000-07:002012-01-19T22:39:13.174-07:00What do insects, plants and skepticism all have in common?They all converge into one singularity of awesome over at <a href="http://botanybugsandbunkum.blogspot.com/">Botany, Bugs and Bunkum</a>. It's a new blog, set up by a good friend of mine. If you're interested in any of the aformentioned subjects then I highly reccomend checking it out!C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-54248150907388519452012-01-18T11:37:00.000-07:002012-01-18T11:37:24.583-07:00A Dispatch from the Science Writing WarsFrom Ed Yong's blog <a href="http://blogs.discovermagazine.com/notrocketscience/2012/01/17/every-scientist-versus-journalist-debate-ever-in-one-diagram/"><i>Not Exactly Rocket Science</i></a>, comes this infographic that pretty much sums up the Scientist vs Science Journalist debate neatly:<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgVY_wmXnRs4LC5my_DGaZG_WI9nSQGNTvbpew55F8NJeBPdx3fqJyZvYQGQw5aiBD2nztM7kQ5BRTIUnZltKbyHJCfWLVVgimULdqfeetZ6VDfzesTQ4_YpMBqPgPbR4Gu_8mhY_fFFNY/s1600/Scientists-and-journalists.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="255" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgVY_wmXnRs4LC5my_DGaZG_WI9nSQGNTvbpew55F8NJeBPdx3fqJyZvYQGQw5aiBD2nztM7kQ5BRTIUnZltKbyHJCfWLVVgimULdqfeetZ6VDfzesTQ4_YpMBqPgPbR4Gu_8mhY_fFFNY/s400/Scientists-and-journalists.jpg" width="400" /></a></div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-89448411980335904372011-10-03T11:00:00.002-06:002011-10-03T11:03:55.941-06:00A Noble Prize and a Noble ConundrumToday the 2011 Nobel Prize in Medicine/Physiology was awarded. This year's Laureates are <b style="font-weight: normal;">Bruce A. Beutler and </b><b style="font-weight: normal;">Jules A. Hoffmann for their discovery of how innate immunity is activated, and to </b><b style="font-weight: normal;">Ralph M. Steinman for his work on how dendritic cells are involved in adaptive immunity. Congrats to all of them!</b><br />
<b style="font-weight: normal;"><br />
</b><br />
<b style="font-weight: normal;">But there's a conundrum here. Steinman, unfortunately, passed away on September 30th. The winners were chosen last week (they are officially announced a week later), and three days later, Steinman died. This presents a problem for the Nobel committee, because the awards are never given out posthumously. Should Steinman still be awarded the prize?</b><br />
<b style="font-weight: normal;"><br />
</b><br />
<b style="font-weight: normal;">I would say yes, and I have a feeling that the committee will make the same decision. Steinman was still alive when the decision was made to award him the prize, and it was only afterwards that he passed away, before the official ceremony. I think that it's likely that the award will be accepted by someone in his place, and Steinman will have the distinction of being the only person to - technically - receive a Nobel posthumously.</b>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-87256223918973842422011-09-30T11:41:00.001-06:002011-09-30T11:41:51.384-06:00Nobel Prizes 2011This Monday (October 3rd) marks the beginning of Nobel Prize season. The prize in Medicine/Physiology is awarded on Monday, with Physics on Tuesday and Chemistry on Wednesday (the Peace prize is awarded on Thursday but who cares about that one?)<sup>1</sup>.<br />
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Any guesses on who will be the lucky Laureates this time around? <br />
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1. No date, as of writing, has yet been set for the prize in Literature. I have not included the Economics prize in this list because it isn't a <i>real</i> Nobel Prize, despite popular opinion that it is.C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-50294703218227176032011-09-30T11:36:00.000-06:002011-09-30T11:36:30.260-06:00Techniques in Molecular Biology: Monoclonal Antibody ProductionAntibodies are perhaps one of the most important tools in the arsenal of molecular biologists. They have a wide variety of applications, from targeting macromolecules with fluorescent dyes or other indicators to aid in visualization, or as a component of other molecular techniques, such as immunopercipitation of proteins. Antibodies that specifically target a researcher's molecule of interest, though, have not always been in the biologist's toolbox.<br />
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Before researchers had this ability, antibodies were produced using a simple technique: inject your antigen of choice into a mouse (or goat, or rabbit), and the mouse will produce antibodies targeted against the antigen. After taking a blood sample from the mouse and collecting the serum, the antibodies could be purified. Antibodies produced in this manner were said to be polyclonal: that is, they were derived from multiple antibody producing B-cells in the spleen. Each antibody producing cell produces a different antibody<sup>1</sup>, and antibodies produced in this way will be a mixture of different antibodies from different cells.<br />
<br />
Monoclonal antibodies, in contrast to the polyclonal variety, are derived from a single antibody producing cell. Antibodies from a single cell will all be specific for the same antigen epitope. This confers several advantages over polyclonal antibodies. Perhaps the biggest advantage is that they allow researchers to target specific epitopes on an antigen. Let's say you wanted to mark a specific residue on a protein using antibodies that are labelled with a fluorescent dye. Using polyclonal antibodies, your protein would end up labelled all over, since the polyclonal antibodies would bind of a variety of epitopes on the protein's surface. Monoclonal antibodies specific to the residue of interest would get rid of all the problematic non-specific binding.<br />
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The production of monoclonal antibodies, however, is somewhat different, and pretty cool. The technique starts off just as it would if you were making polyclonal antibodies: inoculate a mouse using your antigen of interest. The antibody producing B-cells in the mouse spleen will begin to make antibodies that target your antigen. Where Köhler, and Milstein's technique differs is in what is done with those B-cells. Normally, the antibody-producing cells only start making antibodies near the end of their life. Isolating individual cells (thus isolating only one type of antibody) and growing them in culture would work to produce monoclonal antibodies, but only for a short amount of time. Milstein and co. got the idea of fusing the B-cells with immortalized mylenoma cells. Cancer cells can, for a variety of reasons, become immortalized<sup>2</sup>, and continue replicating - indeed, this is what makes cancer a problem! By creating hybrids between B-Cells and mylenoma cells - called hybridomas - they were able to created antibody-producing cells that live forever and keep on producing antibodies. Culturing these cells and purifying the antibodies now became a more viable option. Separate cell lines were isolated and cultured, so that each culture contained only cells from an individual lineage, and consequentially, produced only one kind of antibody. These cells are first grown on plates to establish a lineage, but are eventually transferred to large tissue culture flasks. This allows for tons of monoclonal antibodies to be produced, isolated, and used by researchers the world over.<br />
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This technique pioneered by Milstein and Köhler revolutionized the way research is done in molecular biology. It was important enough that it won Georges Köhler, and César Milstein, the Nobel Prize in Medicine in 1984<sup>3</sup>. Since then, antibodies that target any antigen imaginable have been developed, and can easily be ordered from companies that specialize in production of monoclonal antibodies. It is unlikely, I think, that monoclonal antibodies will be ever displaced as a staple tool for molecular biology research.<br />
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FURTHER READING:<br />
<br />
I you're interested in reading more about the history of antibodies, their discovery and the story of Milstein and Köhler's work, I suggest reading through "A Brief History of the Antibody" posted at the Proteintech Group blog [<a href="http://proteintech.wordpress.com/2011/01/20/a-brief-history-of-the-antibody-part-i/">Part I</a> <a href="http://proteintech.wordpress.com/2011/03/08/a-brief-history-of-the-antibody-part-ii-monoclonal-antibodies/">Part II</a> <a href="http://proteintech.wordpress.com/2011/03/08/a-brief-history-of-the-antibody-part-iii-monoclonal-antibodies/">Part III</a>]. Milstein's Nobel lecture also contains some interesting insights into antibodies, antibody research and the development of Hybridoma technology, and can be found <a href="http://www.nobelprize.org/nobel_prizes/medicine/laureates/1984/milstein-lecture.pdf">here</a>.<br />
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1. The different antibodies produced are specific for the same antigen, but are directed towards different epitopes on the antigen.<br />
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2. This is to say that they are not subject to the Hayflick Limit. The Hayflick Limit, named after American researcher Leonard Hayflick, is the number of times a given cell line can divide before stopping. Originally, cells were thought to replicate indefinitely, and failure to keep cell lines alive was thought to be due to ignorance of optimal techniques. Hayflick and Paul Moorhead, working at the Wistar Institute in Philadelphia in 1961, showed experimentally that cell lines impose a limit on the number of times they can divide. The limit differs between cell types, but for humans it is around 52 divisions. <br />
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3. The prize was shared with Neils Jerne, who was awarded the prize for his work on the development and control of the immune system.C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com1tag:blogger.com,1999:blog-1443345082398372535.post-86987172990892295042011-09-09T21:04:00.000-06:002011-09-09T21:04:02.807-06:00Rick Perry and Galileo: BFFs?With the impending doom that is the Republican presidential nomination looming ominously on the horizon, Wednesday was the night of the latest debate between the Republican candidates. On the list of talking points was the inevitable question about global warming. Denying global warming is <i> de rigueur</i> in the Republican party these days, so it wasn't surprising that, with the exception of Huntsman, the idea of anthropogenic climate change was scoffed at across the board. It was Rick Perry, though, that did manage to raise some eyebrows when he delivered this gem:<br />
<blockquote>"The science is not settled on this. The idea that we would put Americans' economy at jeopardy based on scientific theory that's not settled yet to me is just nonsense...just because you have a group of scientists that have stood up and said here is the fact, Galileo got outvoted for a spell."</blockquote>Oh, Rick, you silly man. How art thou wrong? Let me count the ways:<br />
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1) The science <i>is</i> settled on the issue. Anthropogenic climate change is a reality, one that is accepted by the vast majority of scientists. Some of the exact particulars of the issue are currently under debate - long-term climate projections for the future, the extent to which particular pollutants have contributed, etc - but these are not the things that Perry claims are unsettled. It is the mere existence of anthropogenic climate change that Perry denies, and as far as science is concerned, that issue most certainly is settled. <br />
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2) Galileo was not "outvoted". Perhaps this was just a bad choice of words on Perry's behalf, but I fear that it indicates a deeper misunderstanding of how science works. Scientific debates are not settled by a vote. Scientists are not polled for their opinions and the ideas of the majority put forward as the scientific reality. The "truth" is not determined by popular vote, but by careful and critical consideration of the evidence. I'd like to think that Perry realizes this, but given the anti-science attitude that he and many others in the Republican party display, I'm not so sure that he does.<br />
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3) Does Perry not realize that Galileo's ideas were not suppressed by the scientific community, but rather, by the Church? Perhaps, as a religious conservative himself, Perry has chosen to overlook this fact. Galileo's case does not parallel the criticisms against climate change denialists. Galileo did not meet resistance from the scientific community, for one. The heliocentric model was supported by a large number of Galileo's contemporaries, including Copernicus (who was the father of modern heliocentrism!), Johannes Kepler, and to some extent Tycho Brahe (who had posited his own heliocentric model of the solar system). The condemnation of heliocentrism came from outside the scientific community. It raised the ire of the religious community (much like the concept of global warming does today!). Compare this to climate change. Climate change "skeptics" do not form a large portion of the current scientific community and are largely found on the fringes of science and often in disciplines unrelated to climate change. They are criticized by the scientific community itself, and this in no way parallels the persecution experienced by Galileo. <br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjwd5Txvu9sUpAW03LVsqa5cq34eDs9eYJEMyLhGWvVg2Kx4gtewfd3QPrb9HpVb_JZg4fGq_ek6WAdN0WaXASsQOUQaehF-drxbls0xI1YrsrQHJhpXPTv718sYhoF6SABVqeBryKzC5g/s1600/perry-science.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjwd5Txvu9sUpAW03LVsqa5cq34eDs9eYJEMyLhGWvVg2Kx4gtewfd3QPrb9HpVb_JZg4fGq_ek6WAdN0WaXASsQOUQaehF-drxbls0xI1YrsrQHJhpXPTv718sYhoF6SABVqeBryKzC5g/s400/perry-science.jpg" width="400" /></a></div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-8366259899914011952011-07-22T16:54:00.005-06:002011-07-22T17:00:55.647-06:00Researchers discover "7th and 8th bases of DNA"? Hardly. Here's your daily dose of science journalism fail.<div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">Making the rounds on the blogosphere and the news sites today is the announcement that researchers have discovered the "7th and 8th bases of DNA". This announcement comes from a <a href="http://www.sciencemag.org/content/early/2011/07/20/science.1210597">paper published online on <i>Science</i>'s pre-print server</a><sup>1</sup>, Science Express by researchers at the University of North Carolina School of Medicine, and most of the news reports seem to be based on an <a href="http://www.sciencedaily.com/releases/2011/07/110721142408.htm">article posted to Science Daily</a>. The article reads:</span></div><blockquote style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">"For decades, scientists have known that DNA consists of four basic units -- adenine, guanine, thymine and cytosine. Those four bases have been taught in science textbooks and have formed the basis of the growing knowledge regarding how genes code for life. Yet in recent history, scientists have expanded that list from four to six. Now, with a finding published online in the July 21, 2011, issue of the journal <i>Science</i>, researchers from the UNC School of Medicine have discovered the seventh and eighth bases of DNA."</span></blockquote><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">Oooh! Exciting! What are these bases, exactly?</span></div><blockquote style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">"These last two bases -- called 5-formylcytosine and 5 carboxylcytosine -- are actually versions of cytosine that have been modified by Tet proteins, molecular entities thought to play a role in DNA demethylation and stem cell reprogramming."</span></blockquote><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">So, wait a second. These "new" bases are only modified forms of cytosine? So what? This is no big deal at all. There are well over a dozen known modified bases. Here, let me list a few:</span></div><ul style="font-family: Arial,Helvetica,sans-serif;"><li><span style="font-size: normal;">5-hydroxymethylcytosine</span></li>
<li><span style="font-size: normal;">5-hydroxymethyluracil</span></li>
<li><span style="font-size: normal;">N<sup>4</sup>-methylcytosine</span></li>
<li><span style="font-size: normal;">7-methylguanine</span></li>
<li><span style="font-size: normal;"> N<sup>6</sup>-methylcytosine</span></li>
<li><span style="font-size: normal;">β-D-hydroxymethyluracil</span></li>
</ul><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;">Need I go on? If we're counting modified bases, then there are perhaps two dozen or more known bases. Why do 5-formylcytosine and 5-carboxylcytosine get the elevated status as the '7th and 8th' bases, when there are so many more modified bases that seem to have gone ignored (and who, for that matter, gave 5-methylcytosine and 5-hydroxymethylcytosine the distinction of being the 5th and 6th)?</span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: normal;"><br />
</span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;">Is the discovery of 5-formylcytosine and 5 carboxylcytosine interesting and exciting? Yes, most definitely. Are they the "7th and 8th" bases of DNA? Nope, not at all.</span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><br />
</span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;">--------------------------------------------------------------------------------------------</span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><b>Ito, S., Shen, L., Dai, Q., Wu, S.C., Collins, L.B., Swenberg, J.A., He, C., and Zhang, Y. </b> Tet Proteins Can Convert 5-Methylcytosine to 5-Formylcytosine and 5-Carboxylcytosine. 2011. <i>Science</i> Published Online 21 July 2011 <a href="http://dx.doi.org/10.1126/science.1210597">doi:10.1126/science.1210597</a></span></div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-49369587623959049752011-07-15T21:41:00.001-06:002011-07-16T12:43:26.239-06:00Of Hens Teeth and IDiots.<div style="font-family: Arial,Helvetica,sans-serif;">The literature published by the Discovery Institute often confuses me. I'm never quite sure if it should frustrate me or amuse me. Their constant mangling of science combined with their propensity for telling half-truths and distorting reality both makes me laugh (hah! They really think they have science on their side?) and makes me embittered (How dare they twist science to deceive and miseducate?). I guess this<a href="http://www.evolutionnews.org/2011/07/of_hens_teeth_and_neutral_muta048211.html"> recent article by Discovery Institute crony Casey Luskin</a> should be of no surprise, then. In the piece, titled <i>Of Hen's Teeth and Neutral Mutations</i>, Luskin attempts to dismantle a claim made by Stephen Jay Gould about hen's teeth (or the lack thereof):</div><blockquote style="font-family: Arial,Helvetica,sans-serif;">"Evolutionists often cite an experiment which purportedly induced tooth growth in chickens, supposedly confirming that birds have genes for teeth and are descended from toothed reptilian ancestors. For example, in his book <i> Hen's Teeth and Horse's Toes</i>, Stephen Jay Gould discusses this experiment...But there's a problem with Gould's argument: as Sean Carroll <a href="http://www.ideacenter.org/contentmgr/showdetails.php/id/1432">explains</a>, neo-Darwinism has a 'use-it-or-lose-it' rule. According to neo-Darwinism, if a trait is not used then the DNA which encodes it will accumulate neutral mutations, and eventually the trait will be lost forever. If supposed chicken genes for producing teeth haven't been used for 60+ million years, then that would strongly suggest that neutral mutations should have long-since destroyed their ability to function."</blockquote><div style="font-family: Arial,Helvetica,sans-serif;">For those of you who might be unfamiliar with the experiment in question - and with Gould's discussion of it - it would be worth the while to go into detail. In 1980, Gould published the book <i>Hen's Teeth and Horse's Toes</i>, a collection of articles he had written for various magazines (primarily for <i>Natural History</i>). Included was an article of the same name where he discussed atavisms - apparent reversions in individuals to an ancestral phenotype. Gould claimed that atavisms are a shining example of the evolutionary past of a species coming to the surface. He illustrated his point with two examples: polydactyl horses and chickens with teeth. It is this second example towards which Luskin has aimed his bow and launched forth a volley of ignorance.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">On p.182<sup>1</sup>, Gould explains a curious experiment performed by E.J. Kollar and C. Fisher: they devised a way to prompt chickens to develop teeth. If it's been a while since you took a good look in the mouth of your local avian friends, then it might interest you to know that birds don't have teeth. The most recent known fossil of toothed birds dates to around 80 million years ago, so somewhere in the intervening time, birds lost the ability to produce teeth. Odontogenesis in vertebrates is a complex process (then again, developmental programs always are!). It requires two different tissue types to occur: epithelial tissue and mesenchyme. The outer enamel layer of a tooth is formed by the epithelial tissue, while the inside dentin later of your tooth grows from the mesenchyme. But there's a catch: the mesenchyme cannot produce dentin by itself, it needs to be in contact with epithelium for dentin production to begin - that is to say, epithelium induces the production of dentin. This dentin, in turn, induces the production of enamel in the epithelium. Birds don't produce dentin, nor, consequently, enamel, so birds are born toothless. Kollar and Fisher's idea was brilliant but simple: what happens if you graft chick epithelium with murine (mouse) mesenchyne? Mice most definitely have teeth, so we know their mesenchyne is capable for producing dentin if prompted by epithelial tissue. What they found was astounding: when mouse mesenchyne was grafted to chick epithelium, teeth (dentin and all) were produced. This meant that avian epithelial tissue - despite the fact that birds have no teeth, and have not had teeth for as long as 80 million years - is still able to induce dentin production in the appropriate mesenchyne. Gould mused that this experimental result displayed the evolutionary history of birds. Why else would avian epithelial tissue have the latent ability to induce dentin production unless they had descended from toothed ancestors?</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Luskin, however, thinks that Gould was completely wrong. Luskin argues that, if birds lost the ability to produce teeth 80 million years ago, then the genes for tooth production would have accumulated so many mutations that it would be impossible to revert back to the original toothed phenotype. The tooth production genes, he claims, would have since been destroyed beyond the ability to function. He bases this argument in something called Dollo's Law. Dollo's Law, put simply, states that evolution cannot reverse itself, and that genes which escape selection pressure will degrade fast enough that reverting to the original phenotype is tantamount to impossible. According to Luskin, the example of toothed hens is not the resurrection of a lost developmental pathway but the result of an experimental mistake.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Luskin cites a paper from Marshall, Raff and Raff<sup>2</sup> that seemingly supports his argument. In the paper, the authors devise an equation that determines the probability of a silenced gene's reversion as a function of time passed. They concluded that, for a gene that has been silenced for 10 million years, there is a near-zero probability for reactivation. How do they account for Kollar and Fisher's results? They state that "the classic example of the resurrection of "hen's teeth" is most likely an experimental artifact". Well, that settles it, right?</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Well, no. Marshall, Raff and Raff's paper was published in 1994, and despite what Luskin might think, science has progressed in the two decades since. Perhaps if he had read through more recent literature he would have realized some problems with his argument and with Marshall <i>et al</i>'s conclusion.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">First, let's tackle the "experimental artifact" claim. When Kollar and Fisher's original paper was published, there was some skepticism about their results. There was controversy over whether or not the mouse mesenchyne they used was contaminated with mouse epithelial tissue. If this was the case, then their results would be invalid: it would be impossible to tell whether or not the formation of dentin was prompted by the chick epithelium or the mouse epithelium. Despite the experiment being repeated by other researchers, the possibility of contamination meant that many people wrote off their result as an "experimental artifact". This debate was put to rest, however, by an paper published by Cai <i>et al</i> in 2009<sup>3</sup>. In their paper, the team repeated the tissue graft experiment using mesenchyne from transgenic mice expressing the LacZ gene (LacZ is used in molecular biology as a reporter gene, because it produces a dark blue pigment when supplied the proper substrate). Like Kollar and Fisher, Cai <i>et al</i>'s results showed the induction of dentin by chick epithelium. To prove that there was no contamination by mouse epithelium, they took cross sections of the graft and stained them. The transgenic mouse tissue, expressing the LacZ gene, stained a dark blue while the chick tissue remained unstained. What they found was that the entire epidermal tissue remained unstained, while only the mesenchyne stained blue, ruling out the possibility of contamination. Kollar and Fisher's original results, then, are still valid.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">So if Kollar and Fisher were correct all along, then don't their findings go against Dollo's Law? Shouldn't the genes for tooth production, being free from selective pressures, have accumulated many mutations that would prevent the pathway from functioning at all? The answer, again, is no. Perhaps if Luskin had read the Marshall <i>et al</i> paper more closely (if, indeed, he had read it at all, since he only quotes the abstract) he would have gotten a hint. The authors mention in their discussion that "[r]eversals of long-lost structures do occur but evidently result from the cooption of genes that continue to survive in other roles". In other words, genes involved in traits no longer expressed can avoid the fate of accumulating mutations if they have other roles in development. The genes for tooth production most certainly fit this description. Work by West <i>et al</i> in 1998<sup>4</sup> found that many of the genes required for odontogenesis are still expressed in the developing chick embryo, indicating that they still play important roles. BMP4, for example, plays important roles in muscle development and bone development as well as in the development of teeth. Members of the Hedgehog family of proteins are involved in a whole slew of developmental processes, only one of which is odontogenesis. Toyosawa <i>et al</i><sup>5</sup>, in 1999, looked at one protein in particular, Dentin Matrix Protein 1, or DMP1. Since birds don't produce dentin, what use would they have for such a gene? Toyosawa <i>et al</i> not only found that birds have this gene but found it was being expressed in the jaws of chickens. The case of hen's teeth escapes Dollo's Law because many of them are not silenced, and many of them have other functions in the developing embryo.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">If you think about it, this really should come as no surprise. Dollo's Law describes what happens to single genes that control single phenotypes when they become silenced. Dollow's Law makes no claims about what happens to genes involved in complex developmental pathways. In order for Luskin to be correct, then it would require <i>all</i> the genes in a developmental pathway to have become silenced. Given the interconnected nature of developmental pathways, this simply is not a reality. One or two genes in the pathway may be lost, but the rest remain due to their involvement in other roles. If the missing genes are supplied, then the original, ancestral pathway is reconstructed and the ancestral phenotype is "resurrected". This is precisely what is going on in the example of hen's teeth. The tooth development pathway remains largely intact since many of the genes are involved in other roles. The genes in chick mesenchyne that respond to signals from the epithelial tissue have been lost, which is why birds do not develop teeth. But if you supply these genes in the form of mesenchyne from mice, then the lost pathway is reconstructed and teeth develop. This in no way violates Dollo's Law.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">As for Dollo's Law itself, there is mounting evidence that would indicate apparent exceptions to Dollo's Law might be the rule. In the last ten years, many examples of exceptions to Dollo's Law have been noted, including the evolution of wings in stick insects<sup>6</sup>, the larval stage in salamanders<sup>7</sup>, digit loss in some lizards<sup>8</sup>, egg laying in sand boas<sup>9</sup>, teeth in frogs<sup>10</sup> (which, by the way, have been toothless for 200 million years, more than twice as long as birds), shell coiling in limpets<sup>11</sup>, and even the re-evolution of sexuality in Oribatid mites<sup>12</sup>. As noted by Collin and Miglietta<sup>13</sup>:</div><blockquote style="font-family: Arial,Helvetica,sans-serif;">"with the growing number of phylogenetic studies showing patterns consistent with re-evolution of characters, and genetic data showing that developmental pathways can be maintained for tens of millions of years, is it time to give up Dollo’s Law? Perhaps."</blockquote><div style="font-family: Arial,Helvetica,sans-serif;">So what remains of Luskin's argument but smouldering rubble? Kollar and Fisher's experimental results were not due to experimental error, their results don't violate Dollo's Law, and Dollo's Law itself is on shaky ground. Gould was perfectly correct in referring to hen's teeth as an atavism hearkening back to a bygone day of toothed birds.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Once again, an argument put forth by the ID crowd has failed. Are they incapable of delivering a good argument? It sure seems hard to find one that is the least bit compelling. You might even say they're as scarce as hen's teeth.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">-------------------------------------------------</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">1. Stephen Jay Gould . <i>Of Hen's Teeth and Horse's Toes</i>. 1980</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">2 C. Marshall, E. Raff and R. Raff . Dollo's law and the death and resurrection of genes.<i> Proceedings of the National Academy of Sciences</i>. 1994. <b>91</b>:12283-12287</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">3. Cai J, Cho S-W, Ishiyama M, Mikami M, Hosoya A, Kozawa Y, Ohshima H, Jung H-S. Chick tooth induction revisited. 2009. <i>J. Exp. Zool. (Mol. Dev.Evol.)</i> <b>312B</b>:465–472.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">4. Philippa Francis-West, Raj Ladher, Amanda Barlow, Ann Graveson, Signalling interactions during facial development. 1998. <i>Mechanisms of Development</i>. <b>75</b>(1-2):3-28, DOI: 10.1016/S0925-4773(98)00082-3.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;">5. Satoru Toyosawa, Akie Sato, Colm O'hUigin, Herbert Tichy and Jan Klein. Expression of the Dentin Matrix Protein 1 Gene in Birds. 1999. <i>Journal of Molecular Evolution</i>. <b>50</b>(1), <span class="pagination">31-38</span><span class="doi">, <span class="label">DOI:</span> <span class="value">10.1007/s002399910004</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">6. </span></span><span class="doi"><span class="value">Whiting MF, Bradler S, and Maxwell T</span></span><span class="doi"><span class="value">. </span></span><span class="doi"><span class="value">Loss and recovery of wings in stick insects. </span></span><span class="doi"><span class="value"><i>Nature.</i> 2003 <b>421</b>(6920):264-7.</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value"></span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">7.</span></span><span class="doi"><span class="value"> Chippindale PT, Bonett RM, Baldwin AS, and Wiens JJ.</span></span><span class="doi"><span class="value"> Phylogenetic evidence for a major reversal of life-history evolution in plethodontid salamanders. 2004. </span></span><span class="doi"><span class="value"><i>Evolution</i>. <b>58</b>(12):2809-22.</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;">8. Kohlsdorf T, Wagner GP. Evidence for the reversibility of digit loss: a phylogenetic study of limb evolution in Bachia (Gymnophthalmidae: Squamata). 2006. <i>Evolution</i>. <b>60</b>(9):1896-912</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;">9.<span class="doi"><span class="value">V. Lynch and G. Wagner. Did egg-laying boas break Dollo's Law? Phylogenetic evidence for reversal to oviparity in sand boas. 2010. <i>Evolution</i>. <b>64</b>(1):207-216</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value"><br />
</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">10.Wiens JJ. Re-evolution of lost mandibular teeth in frogs after more than 200 million years, and re-evaluating Dollo's law. 2011 . <i>Evolution</i>. <b>65</b>(5):1283-96. doi: 10.1111/j.1558-5646.2011.01221.x</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value"><br />
</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">11. Collin R, and Cipriani R. Dollo's law and the re-evolution of shell coiling. 2002. <i>Proceedings of the National Academy of Sciences</i>. <b>270</b>(1533):2551-5</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value"><br />
</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">12. Domes K, Norton RA, Maraun M, and Scheu S. Reevolution of sexuality breaks Dollo's law. 2007 . <i>PNAS</i> . <b>104</b>(17):7139-44</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value"><br />
</span></span></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"><span class="doi"><span class="value">13. Collin R, and Miglietta MP. Reversing opinions on Dollo's Law. 2008. <i>Trends Ecol Evol.</i> <b>23</b>(11):602-9</span></span></div><div class="secondary" style="font-family: Arial,Helvetica,sans-serif;"></div><div class="authors" style="font-family: Arial,Helvetica,sans-serif;"></div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-25869499522898808132011-06-23T21:00:00.001-06:002011-06-23T21:06:52.828-06:00$100 worth of science failSo the Canadian government has decided to give our bills a makeover. Gone are the days of money made out of cotton! A new era of synthetic polymer bank notes has arrived. They look pretty cool, which is good. Supposedly, these notes are harder to counterfeit, which is even better. And the $100 bill is a celebration of science, which is even more awesome. The reverse side of the bill shows a bottle of insulin, a lady working at a microscope, and a strand of DNA, as shown below.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_Y_sSpIXeuPk6p4HCj_5qMzUIBuTYbmGTx72XIx2BKjxGC5G7FS9X1pNl7SuM8Uqw9vM_Cii5ojvumXMXIdLGwRouhV3Jt_DtJ1daGE15XChyYonLYHFkW3iDop3y_vWNjyIIDtPIRGo/s1600/sciencefail.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="291" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj_Y_sSpIXeuPk6p4HCj_5qMzUIBuTYbmGTx72XIx2BKjxGC5G7FS9X1pNl7SuM8Uqw9vM_Cii5ojvumXMXIdLGwRouhV3Jt_DtJ1daGE15XChyYonLYHFkW3iDop3y_vWNjyIIDtPIRGo/s640/sciencefail.jpg" width="640" /> </a></div><div class="separator" style="clear: both; text-align: left;"> Wait a second. Something looks wrong here. Let's take a closer look...</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjAULEooHaQzTTuOVM5ZXuSpIgnW1bpXNKxvSll937SicEjNOZRqhZ6Xa8azZvHEqY2wfjPfe8x1XSN8fzJ5xOhA-wJd2jcReSruaj9eii4GJneEk49MzclB_M6Bb5imvZNwU-IXlQTtjw/s1600/moneyfail.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="292" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjAULEooHaQzTTuOVM5ZXuSpIgnW1bpXNKxvSll937SicEjNOZRqhZ6Xa8azZvHEqY2wfjPfe8x1XSN8fzJ5xOhA-wJd2jcReSruaj9eii4GJneEk49MzclB_M6Bb5imvZNwU-IXlQTtjw/s640/moneyfail.jpg" width="640" /></a></div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;"> That helix is left-handed! DNA is a right-handed helix, not a left-handed helix. I applaud the Government for making the bill science-centric, but really, how hard would it have been to get the art accurate? <a href="http://www-lmmb.ncifcrf.gov/%7Etoms/LeftHanded.DNA.html">The left-handed helix mistake is incredibly common</a>, but that's really no excuse. </div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com4tag:blogger.com,1999:blog-1443345082398372535.post-7448196690381080752011-06-16T14:57:00.000-06:002011-06-16T14:57:07.924-06:00Wait...what?Where do I even begin with this one?<br />
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<object style="height: 390px; width: 640px;"><param name="movie" value="http://www.youtube.com/v/JYV0M6Y41Go?version=3"><param name="allowFullScreen" value="true"><param name="allowScriptAccess" value="always"><embed src="http://www.youtube.com/v/JYV0M6Y41Go?version=3" type="application/x-shockwave-flash" allowfullscreen="true" allowScriptAccess="always" width="640" height="390"></object><br />
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You know what? I'm just going to let this picture do the talking.<br />
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<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgCicpmoFxOmEv4wUqSvMlVcBCiGKyFQXhE-lYwjE_v7uetfEwZyPZi0dBUNG39PQ1p2QrrwMpjXTAJ-gt0MCcPvLSyVuqlaoZmH5K-hxDyIqrlhMRnxQj-92HaQH7j8dtYoaL7swt3zj8/s1600/thestupiditburns.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgCicpmoFxOmEv4wUqSvMlVcBCiGKyFQXhE-lYwjE_v7uetfEwZyPZi0dBUNG39PQ1p2QrrwMpjXTAJ-gt0MCcPvLSyVuqlaoZmH5K-hxDyIqrlhMRnxQj-92HaQH7j8dtYoaL7swt3zj8/s320/thestupiditburns.jpg" width="280" /></a></div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-25124720779669773842011-06-09T22:12:00.002-06:002011-06-09T22:15:11.023-06:00OM NOM NOM<div style="font-family: Arial,Helvetica,sans-serif;">From the journal <i>Entomological Science</i> (published online May 18th) comes this interesting predator-prey role reversal<sup>1</sup>:</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
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</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLO4VKqDuf9Fap9fLRE1BGb6Hz2-aTB4QnqPaAaebclEZFgk7JkiKThH5iZddjljDS7Ox8SSEDh3NWEOmKW-1l4BrlPQ29bdwe9QArGCUK6XcAQOwTIFsJGpGkOovC6myr5Rn7TVh-f24/s1600/insect-eating-turtle.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="223" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiLO4VKqDuf9Fap9fLRE1BGb6Hz2-aTB4QnqPaAaebclEZFgk7JkiKThH5iZddjljDS7Ox8SSEDh3NWEOmKW-1l4BrlPQ29bdwe9QArGCUK6XcAQOwTIFsJGpGkOovC6myr5Rn7TVh-f24/s400/insect-eating-turtle.jpg" width="400" /> </a></div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: center;"><br />
</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">Yes, that is a giant water beetle eating a turtle.</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"><br />
</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">The photo was snapped by Shin-ya Ohba outside of Hyogo, Japan, while collecting samples for his research. While giant water beetles are known to chow down on smaller insects and small fish, finding one dining on a baby turtle is quite bizarre. Ohba writes:</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"></div><blockquote><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">"The bug inserted his proboscis into the neck of the turtle....Although I could not confirm whether the bug caught the turtle by himself in this observation, the dead body of the turtle was fresh. Probably, he had just captured the turtle. This is a first report of a Lethocerinae eating a turtle."</div></blockquote><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"></div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"></div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"></div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">Pretty neat. And also pretty scary.</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"><br />
</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">--------------------------------------------------------------------------------------------</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;">1. S. Ohba . "Field observation of predation on a turtle by a giant water bug" . 2011 . <i>Entomological Science</i> . doi:10.1111/j.1479-8298.2011.00450.x </div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: left;"><br />
</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-69317590340647867522011-06-05T23:14:00.000-06:002011-06-05T23:14:16.985-06:00This Week in Science (June 5, 2011)Just a pair of papers for this week's TWIS. I haven't had much time to dedicate to reading new research this week, but I'll have more next week!<br />
<br />
To start off, I'll <a href="http://www.sciencemag.org/content/332/6034/1163.full">point you in the direction of the infamous "arsenic bacteria" paper</a>, which has finally been published in <i>Science</i> after languishing on <i>Science</i>'s pre-print server for months. This paper, if you're unfamiliar with it, claimed to show the discovery of a new species of bacteria that utilized arsenic in its DNA rather than phosphorus. It was torn to shreds by critics due to problems in the authors' methodology and doubts about the results - <a href="http://cwgk.blogspot.com/2010/12/arsenic-life-zomg-straight-dope-on.html">and for good reason</a>. <i>Science</i>'s response to all the negative criticism that the paper has recieved has been to publish a list of criticisms (and the authors' responses) along with the paper. <a href="http://whyevolutionistrue.wordpress.com/2011/06/05/the-arsenic-paper-is-out-along-with-eight-critiques/">Jerry Coyne has a good rundown of the paper's publication on his blog</a>. <br />
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Continuing on:<br />
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<ul><li><b>DNA computing and square roots</b> - Published this week in <i>Science</i> is a paper by L. Qian and E. Winfree detailing an interesting advancement in DNA computing. The authors were able to design and string together DNA logic gates to create a simple molecular computer able to calculate square roots. Creating a DNA logic gate is actually quite simple, and there are multiple ways it can be done. The authors did it by using a "seesaw gate"design: the gate consists of a short stretch of DNA that can pair with multiple different sequences. One such sequence is added as an "input", which competes and replaces a second sequence that is already bound to the gate. This replaced sequence becomes the "output", which is then free to act as an input for a second gate. Gates can be strung together to create more complicated systems. The authors devised a way to string such gates together to create a system that could calculate square roots. As cool as this is, though, this early biological calculator takes a while to complete calculations - up to eight hours. Nevertheless, this is a big step towards creating bigger and more powerful DNA computers. A more detailed summary of the paper has been <a href="http://www.wired.com/wiredscience/2011/06/dna-mathematics/">posted on Wired</a>, which I highly recommend, as they do a better job explaining logic gates than me!</li>
</ul>(L. Qian and E. Winfree . "Scaling up digital circuit computation with DNA strand displacement cascades" . <i>Science</i> . 2011 . <b>332</b>(6034): 1196-1201, doi: <span class="slug-doi" title="10.1126/science.1200520">10.1126/science.1200520)</span><br />
<br />
<ul><li><span class="slug-doi" title="10.1126/science.1200520"><b>Proteins successfully extracted from mammoth bones</b> - A paper published <strike>this week</strike><sup>1</sup> in the journal </span><em>Geochimica et Cosmochimica Acta</em><span class="slug-doi" title="10.1126/science.1200520"><b> </b>describes the successful extraction of collagen protein from 600,000 year old mammoth bones. The authors were investigating the idea that peptide mass spec. could be used to identify fossils; that is, if you could determine the sequence of proteins in the fossil, you could compare the sequences to a database of known proteins. Finding proteins which are a close match would narrow down the identity of the fossils in question. To test this idea, the authors used bones from two mammoth fossils and one mastodon fossil. After grinding samples of the fossils into powder, they performed a series of chemical extractions and washes, then prepared them for mass spec. This allowed them to sequence the extracted protein, which was confirmed as collagen. The sequence data was good enough that the collagen - and consequently, the fossils - were correctly identified as being related to elephants. The authors were even able to use this data to distinguish the samples as </span>elephantid (mammoth) or mammutid (mastodon). These findings are important for two reasons: first, they show that proteins can successfully be recovered from fossils as old as 600,000 years; and secondly, they demonstrate that protein mass spec. can be used to correctly identify ancient fossils (or at the very least, identify the closest living relative). Exciting indeed!</li>
</ul>(M. Buckley, N. Larkin, and M. Collins . "Mammoth and Mastodon collagen sequences; survival and utility" . Geochemica et Cosmochimica Acta . 2011 . <b>75</b>(7): 2007-2016<br />
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1. This paper actually wasn't published this week, it was published in April. For whatever reason, it looks like it only made the news now.C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-39576824432271775822011-05-29T03:51:00.002-06:002011-05-31T01:37:38.166-06:00Fir-Tex: Bullshit in vest form.Move over Q-ray, there's a new nonsense product in town.<br />
<br />
Everyone is familiar with Q-Ray bracelets. Little more than two ball bearings attached with a piece of steel cable, Q-Ray bracelets are marketed as some sort of mystical device that will revitalize your "bio-energy" (whatever that means). <a href="http://cwgk.blogspot.com/2008/01/q-ray-ionized-bracelet-more-like.html">Despite being a known fraud</a>, the Q-Ray bracelet remains popular. In the face of mounting evidence that it's a load of baloney, we've seen the nonsense "bio-energy" fad expand in the last year. Products like the phony Power Balance bracelets have hit the market (and like the Q-Ray before it, have been debunked a thousand times over by the skeptic community). But if you've ever said to yourself "I really wish I had a similar product that covered my entire torso", then you've been out of luck.<br />
<br />
Until now.<br />
<br />
<a href="http://fir-tex.com/en/">Introducing "Fir-Tex", the latest in wallet-draining pseudoscientific technology</a>. Fir-Tex claims to be the first "energized textile", that can be fashioned into clothing. Products such as <a href="http://www.wearwings.com/">Wear Wings</a> - brought to you by Red Bull - are being marketed as the world's first in "energy fashion". Having a slow day? Feeling drained at work? Don't worry, just send in a big cheque, pull a Fir-Tex vest on over your body and your motor will be revving like a chihuahua on speed.<br />
<br />
But how does it work? Or better yet, <i>does</i> it work?<br />
<br />
<span style="font-size: large;"><b>Bold Claims </b></span><br />
Before we get into the "science" behind Fir-Tex, let's take a look at just what the product has been claimed to do. A banner at the bottom of the Fir-Tex splash page tells us that Fir-Tex clothing will "improve energy and wellbeing", allow you to "jump 10% higher", "improve performance", "boost power by 10%" and "optimize balance and microcirculation". These claims are pretty generic as far as "energized" products go. You'll see similar claims made for Power Balance and Q-Ray bracelets. Also note that claims like these are incredibly ambiguous. What exactly does "improved wellbeing" mean? How do you "optimize" microcirculation? How do you "boost" power, and for that matter, how do you measure power in order to determine that it's been boosted? These claims are little more than technobabble; they're utterly meaningless strings of sciency-sounding words. Just how ridiculous the Fir-Tex gobbledygook is can easily be illustrated. Of the following three items, one is related to Fir-Tex and the other two are taken from Star Trek. Can you tell which is which?<br />
<ul><li>decyon field fluctuations</li>
<li>biogenic energy in the 40 to 50 micron range</li>
<li>aggregate field of plain polarization</li>
</ul>Fir-Tex stops short of making any sort of medical claims, however. They're probably aware of how Q-Ray's medical claims worked out (very poorly), and to avoid lawsuits, they've added a disclaimer to their site:<br />
<blockquote>"So by entering this website you must first acknowledge that FIR-TEX has not been designed for and does not make any claims whatsoever to be any kind of medical cure. Because it isn’t! The aim of FIR-TEX is to bring technological fabrics on the market and their products will help some subjects to simply perform better or feel better while others won't experience any difference or could even feel discomfort."</blockquote>So despite their claims of "increased performance", they acknowledge that "others won't experience any difference". How convenient. If Fir-Tex doesn't work for you, it doesn't mean the product is a fraud, it just means that you're different.<br />
<br />
But enough about bogus product claims, let's get down to some science. <br />
<br />
<span style="font-size: large;"><b>Im in ur body vibratin ur waterz</b></span><br />
So how does Fir-Tex work? Luckily for us, the Fir-Tex site has a science section. According to their site, Fir-Tex works on the principle of Far Infrared Rays. These are energetic rays that lay just outside the visible spectrum. They have wavelengths greater than that of visible light, but shorter than that of microwaves. What do far infrared rays do? Well, I'll let the Fir-Tex folks explain it to you:<br />
<blockquote>"The human body is a reservoir of all kinds of bio-toxins which cannot be expelled immediately and become stored in the body, thereby triggering illness. When toxic gases such as sulfur dioxide and carbon dioxide, or potentially fatal heavy metal toxins such as mercury, lead and chlorine, meet large water molecules, they are encapsulated by clusters of water and trapped in the body. Where these toxins are accumulated, blood circulation is blocked and cellular energy is impaired. However, when a 7 to 11 micron FIR wave is applied to these large water molecules, the water begins to vibrate. This vibration reduces the ion bonds of the atoms which are holding together the molecules of water. As the water evaporates, the encapsulated gas and toxins can be released and this is exactly what FIR technologies can do for the human body."</blockquote><br />
Wait....what? It took me a few times to read that paragraph to understand what they're trying to say. From what I understand, it's this: "bio-toxins" accumulate in your body by being "encapsulated" by water, and causing illness. FIR "vibrates" the water, "reducing" the ion bonds, causing the water in your body to evaporate and setting the toxins free so they can be expelled from the body.<br />
<br />
<br />
<br />
This paragraph also represents a massive chemistry fail. When toxins enter your body, they do not become "encapsulated" by water molecules. This is another instance of technobabble - water cannot "encapsulate" anything, let alone toxins<sup>1</sup>. Perhaps they mean that toxins will bind with water molecules, but this won't happen either. Water molecules won't bind with gasses, nor will water bind with mercury.<br />
<br />
The paragraph continues to tell us that applying far infrared rays to water, the molecules will vibrate, and this vibration "reduces the ion bonds". They're correct in stating that applying far infrared rays will cause the water molecules to vibrate; this is because applying ANY kind of energy will make water molecules vibrate. Think back to junior high chemistry class. When you apply energy to molecules, what happens? They speed up, move around faster, begin to vibrate more. If you put a glass of water in the microwave, what will happen? It boils. The microwave radiation increases the energy of the water molecules and they start moving faster and faster. Applying infrared radiation is no different - it increases the energy of the water molecules and they will move around faster. This is the whole idea behind the <a href="http://en.wikipedia.org/wiki/Infrared_heater">infrared heat lamps</a> you see keeping the burgers warm at McDonald's. So while infrared rays will make water vibrate, they aren't special in their ability to do this.<br />
<br />
Furthermore, even though infrared heat can get water vibrating faster, it won't "reduce the ion bonds of the atoms which are holding together the molecules of water" because <i>water does not contain ionic bonds</i>. All bonds are not the same. Some bonds have more energy than others. Some bonds are made by sharing electrons between atoms, while some are made by the transfer of an electron from one atom to another. The different types of chemical bonds are given different names to distinguish them from one another. Ionic bonds are once such type of bond. They're formed by the electrostatic attraction of two differently charged ions. Sodium ions and chloride ions will forms ionic bonds and produce salt, for example. Water does NOT form ionic bonds. Water forms hydrogen bonds. These are a very different type of bond. <br />
<br />
But perhaps that's just semantics. The point Fir-Tex makes is that applying far infrared rays will make the water molecules in your body evapourate, and allow toxins to be removed. Now, if you don't immediately see how that incredibly terrible that is, then read it again. Let's ignore the fact that it would take an extraordinary amount of radiation to make the water molecules evapourate. Considering how important water is for the proper functioning of your body, does evapourating the water from your very tissues sound like a good idea? And, if the water is supposedly "encapsulating" toxins, wouldn't freeing them from the ensnaring water molecules be even worse? Then they would have free reign to move about your body. Take mercury as an example, since it is one of the toxins mentioned by Fir-Tex above. Mercury does its damage by accumulating in neurons and inhibiting the formation of <a href="http://en.wikipedia.org/wiki/Myelin">myelin</a>. At high concentrations, it can cause severe impairment of mental faculties and can potentially be fatal. If mercury were "encapsulated" by water molecules in the blood, it would actually prevent mercury from reaching your central nervous system and doing damage. Fir-Tex products would actually be doing more harm than good!<br />
<br />
It's also interesting to note that Fir-Tex is not the only "far-infrared technology" on the market. However, Fir-Tex does claim to be "different" from all those other products. How is it different? Well, Fir-Tex doesn't seem to want us to know:<br />
<blockquote>"During our meetings with our customers we explain the difference between our product/technology and any other product using FIR technologies. The technical information is not public for the moment for obvious reasons which one would of course understand."</blockquote>No, actually, I don't understand.<br />
<br />
So the principle by which far-infrared technology is supposed to rely on is nonsensical at best and utterly batshit-stupid at worst. Does Fir-Tex have any evidence that it works?<br />
<span style="font-size: large;"><b><br />
</b></span><br />
<span style="font-size: large;"><b>Science, schmience. We use Chinese medicine!</b></span><br />
The Fir-Tex website's science section has a page called "Live Blood Analysis", which they present as scientific evidence that their product works. I'll get to that in the following section. What I want to go through first is <a href="http://fir-tex.com/docs/FIRVEST-SCIENTIFIC-PRESENTATION.pdf">this "scientific presentation"</a> that can be found on their website. <br />
<br />
The presentation begins with a summary of infrared rays. They claim that infrared rays are "most beneficial" for "the living beings". In what ways they are "most beneficial" is not explained. They do, however, give three properties of infrared rays. First, they "can generate heat by direct irradiation but localized objects can also reflect them". Well, so can microwaves, but sitting next to a microwave tower is a bad idea. In fact, that's WHY it's a bad idea. Secondly, they "deeply penetrate the living tissues". Well, so can X-rays, but again, basking in X-rays isn't a good idea either. And finally - and this one's a doozy - they "activate (water) molecules, increasing overall temperature of the system". Increasing the overall temperature of the system is the same thing as generating heat, mentioned in the first point. But what does it mean to "activate" water molecules. Are all the water molecules in your body normally "inactive"? How do they become "active" in the presence of infrared rays? This is yet more technobabble (sensing a theme here?). These three properties, Fir-Tex says, are why far infrared rays are called “bio-genetic rays” (another made-up word).<br />
<br />
Continuing on, Fir-Tex evokes Wein's displacement law as some sort of justification for their claims. Wein's Law takes the form of λ=K/T, where T is temperature in degrees Kelvin, λ is wavelength in nm, and K is a constant, equal to about 2.896x10<sup>-3</sup>m.K. Using this equation, Fir-Tex calculated the "frequency of emitted radiation" at 35°C as 9.4μm. If you whip out your calculator, you'll see that their math checks out. Human bodies (at 37°C, not 35°C, but whatever) do emit infrared heat at about 10μm, and this is what IR cameras are calibrated to measure. Armed with this number, what does Fir-Tex do? They conclude that "this explains why human body [sic] easily absorbs far infrared rays between 4 and 16 microns". Holy non sequitor, Batman! Using Wein's law shows what wavelength the human body <i>emits</i>, but says nothing about what wavelength it <i>absorbs</i>. And even if it did show that the body absorbs light of a certain wavelength, how does that show it is the "most easily" absorbed wavelength? What would that even mean?<br />
<br />
What does any of this have to do with Fir-Tex's brand of far infrared technology? Well, as the presentation points out, our bodies are composed of large amounts of water. Infrared radiation can make water warmer. Fir-Tex<br />
<blockquote>"works like an active mirror; it captures/receives the thermal radiations from the body heat. Then it reacts and uses these thermal/Far Infrared rays (rays of life) to send energy back into the body with multiple beneficial consequences on cells and tissues."</blockquote>In other words, Fir-Tex is the world's most expensive blanket! All it purports to do is trap the heat radiated by your body. The same effect can be achieved by a wool blanket. $30 at Bed Bath and Beyond and you can be soaking in all the Rays of Life (whatever <i>that </i>means) that you want.<br />
<br />
But Fir-Tex is firm in their belief that infrared radiation is beneficial. Afterall, it's what Qigong masters use!<br />
<blockquote>"Energy medicine is very old, at least as old as the first Qigong masters and other ancient practitioners of healing touch therapies. These healers all had in common the ability to emit energy through their hands, and so do many modern day healers, such as Dolores Krieger, Ph.D., R.N., who began teaching healing touch techniques in the U.S. in the 1970s. Contemporary researchers have now proved that these forms of energy medicine use wavelengths in the infrared range."</blockquote>Qigong "healers'" hands emit radiation in the infrared range? Does this come as a surprise to them? That's the range at which <i>everyone's</i> body emits radiation. That's what the Wein's equation above showed!<br />
<br />
But none of this actually shows that Fir-Tex works at all. Fir-Tex's supposed evidence can be found in the <a href="http://fir-tex.com/en/science/">Live Blood Analysis section of their Science page</a>. <br />
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<span style="font-size: large;"><b>Live Blood Analysis, or How Not to do a Scientific Study</b></span><br />
Prior to this, I had not heard of Live Blood Analysis (LBA). I'm more than familiar with haemotological techniques, but Life Blood Analysis was not a technique that I knew. A few minutes on Google, and I discovered that LBA is a technique pioneered by a company called <a href="http://www.sevenpointfive.co.za/">Sevenpointfive</a>. Who's Sevenpointfive, you ask? They're a South African naturophathic company that pushes their brand of "natural supplements". They present the same, tired "modern medicine is wrong, buy our products instead" line as every other "natural supplement" company. Their schtick, though, seems to be their LBA technique. What they do is simple. They take a drop of your blood, and look at it under a microscope for "imbalances" and "deficiencies". Whether or not Sevenpointfive's "technicians" can accurately diagnose physiological conditions using LBA is rather dubious to me. As far as I can tell, LBA is not a proper technique used by the medical community.<br />
<br />
It's this exact method that Fir-Tex used to test their product. They took blood samples of individuals, then gave them all Fir-Tex vests to wear for 10 minutes, and took another sample. Then they compared the two. That is as detailed as their test gets. There's a huge problem here: they didn't use a negative control subject (or if they did, they never mentioned it or showed the results)! This is a gigantic experimental flaw, and any results from their tests are worthless because of it. They also make no mention of what kind of activities the subjects were doing when they were using the Fir-Tex vests? Were they sitting still for ten minutes? Were they exercising? Was this controlled at all? Their methodology is severely lacking. Such a study would <i>never</i> get published in any reputable medical journal, which is probably why it exists only on the Fir-Tex website. <br />
<br />
What were the results of their "tests"? Well, I haven't the slightest clue. Take a look at what they present as evidence:<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiNwwRGl72e9LcwZge49WcXtK81GfpsQtCKw7zcqWAuAewx4JwE4L-1MIf5hdlUreM7rnyr3qX58V1qSm4hu8vagv3fBkodOgeVccuoji866teek-7wLS9Wzyp1bmCCnsJXe59dfmbH9Ec/s1600/LBA.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="311" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiNwwRGl72e9LcwZge49WcXtK81GfpsQtCKw7zcqWAuAewx4JwE4L-1MIf5hdlUreM7rnyr3qX58V1qSm4hu8vagv3fBkodOgeVccuoji866teek-7wLS9Wzyp1bmCCnsJXe59dfmbH9Ec/s400/LBA.jpg" width="400" /> </a></div><div class="separator" style="clear: both; text-align: center;"><br />
</div>Maybe it's because I don't have sufficient training to understand what I'm looking at, but I don't see a significant difference in the two treatments. All I see are alot of erythrocytes with some platelets here and there, in both cases. Nevertheless, Fir-Tex claims results like these indicate that their product protects cells from damage from free radicals (free radicals, according to Fir-Tex, are "atoms that are missing ions", a laughably stupid statement), reduces cholesterol, and boosts the immune system. None of their LBA pictures indicate any of these things. It is interesting to note that Fit-Tex admits "that each individual reacts differently to the same treatment, the results are thus never the same", but they don't accept this as evidence that their product does nothing. Quite to the contrary, they take this as evidence that Fir-Tex does work, just in different ways in different people. These tests definitely do not bolster their earlier claims of increasing your jump height by 10%, or "optimizing your balance". And even if they DID show such results, we have no way of knowing any of this is attributable to the Fir-Tex vests because of their shoddy methodology! <br />
<br />
No doctor worth their medical degree would produce a medical study as awful as this. So who is responsible? Fir-Tex informs us that the tests were performed by "Dr Annelise Bunce, certified Clinical Metal Toxicologist and certified Dark Field and Multi Phase Microscopy and expert in Live Blood Analysis". <a href="http://www.fir-tex.com/docs/Annelise%20Bunce%20CV.pdf">Here is her CV</a>. Masters in <i>homeopathy</i>? Oooh. That explains it.<br />
<br />
<span style="font-size: large;"><b>More money than sense</b></span><br />
<a href="http://www.firtexshop.com/en/">So just what will one of these babies set you back</a>? Between <span class="price-including-tax"><span class="price" id="price-including-tax-186">€325 and </span></span><span class="price-including-tax"><span class="price" id="price-including-tax-186">€475 (that's $453CAN to $663CAN). Hell, while you're at it, </span></span><span class="price-including-tax"><span class="price" id="price-including-tax-186">€525 will <a href="http://fir-tex.com/en/animals/">get you a saddle for your horse</a>. This is an unbelievably colossal waste of money. Fir-Tex does nothing more than make you warm. The "science" behind it is complete and utter nonsense, none of their claims can be validated and it simply <i>does not work</i>. Just like the Power Balance and the Q-Ray before it, Fir-Tex is a scam that will have its manufacturers laughing all the way to the bank.</span></span><br />
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<br />
<span class="price-including-tax"><span class="price" id="price-including-tax-186">------------------------------------------------------------------------------------</span></span><br />
<span class="price-including-tax"><span class="price" id="price-including-tax-186">1. It's been brought to my attention that this point is not entirely correct. Water molecules can, in fact, "encapsulate" some ions. This is called a "solvation shell". It occurs when a positively charged ion is attracted to the electrostatically negative oxygen of water molecules. Water molecules will effectively form a shell around the ion. I have my doubts about whether water can form a solvation shell around toxins, which are rather large compounds. Perhaps a more chemistry-minded reader could clarify this. </span></span>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com6tag:blogger.com,1999:blog-1443345082398372535.post-38176082542271588062011-05-26T20:26:00.000-06:002011-05-26T20:26:02.163-06:00Central Dogma not so challenged after all?<div style="font-family: Arial,Helvetica,sans-serif;">In last week's <a href="http://cwgk.blogspot.com/2011/05/this-week-in-science-may-22-2011.html">This Week In Science</a>, I summed up a paper published in <i>Scicence</i> by Li <i>et al</i>.<sup>1</sup> which was hyped up as being a challenge to the Central Dogma of molecular biology. The authors compared the RNA sequences from numerous individuals to the original DNA sequences they were derived from. What they found were a multitude of sites where the RNA sequences differed from that which would be expected given the original DNA sequence. Moreover, these variations were shared across individuals, indicating that they were not likely due to random mutation. Furthermore, the team found proteins that matched the varied RNA sequences and not the DNA sequences. These results suggested that there exists some yet unknown editing step during transcription that alters individual nucleotides in the resulting RNA transcripts.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">However, declaring the Central Dogma to be toppled may have been a bit premature. According to Lior Pachter at the University of California, Berkley, the variations discovered by the researchers could be artifacts caused by their sequencing equipment. Many of the sites that were found to contain altered nucleotides lie in regions which are known to often cause RNA sequencing errors. In other words, the variations that the team observed, in many cases, might just be sequencing mistakes. </div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Further skepticism has been <a href="http://www.genomesunzipped.org/2011/05/notes-on-the-evidence-for-extensive-rna-editing-in-humans.php">shown by Joe Pickrell at the blog Genomes Unzipped</a> (which I highly suggest reading, as he goes into quite a bit more detail than what I've presented below). He points out that the differences in RNA and DNA that the authors discovered might be false positives created by attributing a particular RNA sequence to the incorrect DNA sequence. For any given DNA sequence, there are bound to be other sequences very similar - even almost identical - to it<sup>2</sup>. If you are given an RNA sequence, then, how do you determine which of the very similar DNA sequences it is derived from? Unless one takes steps to remove the incorrect sequences, it is very likely that you will end up with a false-positive. It would appear that Li <i>et al</i>. did not take such steps. </div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Pickrell points out another problem with sequencing and mapping through RNA splice sites. Mammalian genes are frequently alternatively spliced, and a cDNA library like the ones Li <i>et al.</i> used will have multiple isoforms of a gene. When mapping such transcripts back to the genome, you have to keep in mind that the genomic sequence will still contain the introns that have been excised in the mature mRNA transcripts. If you compare the shorter, edited mRNA to the longer, unedited DNA, you're likely to find many differences between the two. Mapping a particular sequence read to the wrong isoform will generate false-positives. Pickrell shows that Li <i>et al.</i> did just this on at least one occasion.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">So widespread RNA editing in humans might not be a reality. It's possible that it is, but problems with the procedure used by <i>Li et al.</i> raise many doubts. I'm looking forward to reading the follow-up research. Until then, as perhaps Mark Twain would say, reports of the death of the Central Dogma have been exaggerated. </div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">----------------------------------------------------------------------------------</div><div style="font-family: Arial,Helvetica,sans-serif;">1. M. Li <i>et al</i>. "Widespread RNA and DNA sequence differences in the human transcriptome". 2011. <i>Science</i>. doi:10.1126/science.1207018</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">2. It should be obvious that the larger the given sequence, the fewer (near)identical sites there will be.</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-59383259814632046722011-05-24T01:19:00.002-06:002011-05-24T01:29:06.442-06:00This Week in Science! (May 22, 2011)<div style="font-family: Arial,Helvetica,sans-serif;">This week<sup>1</sup> saw quite a few interesting papers in biology. Here's a few that caught my attention:</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><ul style="font-family: Arial,Helvetica,sans-serif;"><li><b>Mammalian brain evolution driven by smell</b> - One of the biggest characteristics that distinguish mammals from other animals is that we have relatively large brains in relation to body size. Just why mammals evolved rather large brains has been a point of speculation, but a paper published in <i>Science</i> this week suggests that a reliance on our sense of smell resulted in our bulging brains. The research by T. Rowe <i>et al</i>. involved examining the fossils of two species of Jurassic cryodonts, the group of ancient reptiles which would diverge to become the mammalian lineage. They used a technique called X-ray computed tomography to reconstruct endocasts of the cryodont brains, and compared them to those of earlier, Triassic cryodonts. They first looked at the endocast from <i>Morganucondon oehleri</i>, and noted that the brain was 50% larger than in earlier cryodonts. But there were other important differences: the olfactory bulbs were larger, there was expansion in the cerebral hemisphere, and the cerebellum extended to cover the midbrain. They next looked at the endocast from <i>Hadrocodium wui</i>, the closest known fossil to living mammals. They observed another 50% increase in brain size, with even larger cerebral hemisphere and olfactory bulbs. These observations lead the team to speculate that increased dependence on olfaction drove the evolution of larger brain sizes in early mammals. Given that early mammals were likely nocturnal, and had to rummage around in the dark for food, this idea does make sense. The researchers are now looking for evidence that might indicate that early mammals were indeed nocturnal. </li>
</ul><span style="font-family: Arial,Helvetica,sans-serif;">(T. Rowe </span><i style="font-family: Arial,Helvetica,sans-serif;">et al</i><span style="font-family: Arial,Helvetica,sans-serif;">. "Fossil evidence on origin of the Mammalian brain" 2011. Science. </span><b style="font-family: Arial,Helvetica,sans-serif;">332</b><span style="font-family: Arial,Helvetica,sans-serif;">(6032): 955-957)</span><br />
<ul style="font-family: Arial,Helvetica,sans-serif;"><li><b>Another strike against the Central Dogma</b> - Every student in biology is brought up to know the "Central Dogma" - the idea that can be summed up as "DNA encodes RNA encodes protein". This is not a had and fast rule, though, and the discovery of things like ribozymes have shown the Central Dogma to be less dogmatic. A new paper published in <i>Science</i> this week furthers this point. A team of researchers lead by M. Li from the University of Pennsylvania in Philadelphia compared the DNA sequences from 27 different individuals to their corresponding RNA sequences. In a very large number of cases, they discovered that the RNA sequences that had been transcribed from the DNA sequences were different than would be expected; that is, the RNA sequences contained sites where the nucleotides had been changed. These changes in RNA sequences were shared across many of the individuals studied, indicating that the changes were not likely due to random mutation. Furthermore, using mass spectroscopy, they found peptides whose sequences reflected the RNA variant sequences rather than the original DNA sequences. What all of this suggests is that the DNA-RNA-Protein relationship is not as strict as previously thought. The DNA sequence of a gene might not dictate the exact composition of it's gene product after all. </li>
</ul><span style="font-family: Arial,Helvetica,sans-serif;">(M. Li </span><i style="font-family: Arial,Helvetica,sans-serif;">et al</i><span style="font-family: Arial,Helvetica,sans-serif;">. "Widespread RNA and DNA sequence differences in the human transcriptome". 2011. </span><i style="font-family: Arial,Helvetica,sans-serif;">Science</i><span style="font-family: Arial,Helvetica,sans-serif;">. doi:10.1126/science.1207018)</span><br />
<ul style="font-family: Arial,Helvetica,sans-serif;"><li> <b>Extinction rates may be overestimated</b> - Estimating extinction rates is an important part of ecological conservation, but unfortunately, there is really no reliable way of directly determining such rates. Instead, researchers often rely on indirect methods, but this can run into problems. One popular indirect method is to observe the number of different species found as your area of study gets larger (called a species-area accumulation curve), and then extrapolating backwards to successively smaller and smaller areas to determine the rate at which species number decreases. A new paper in Nature by Fangliang He and Stephen Hubbell argue that this method routinely overestimates extinction rates (sometimes by as much as 160%!). This comes as both good news and bad news; it means that species loss due to habitat destruction in some areas might not be as high as previously estimated, but it also means a more accurate method for estimating extinction rates needs to be devised in order to develop optimal conservation projects. </li>
</ul><div style="font-family: Arial,Helvetica,sans-serif;">(F. He and S. Hubbell. "Species-area relationships always overestimate extinction rates from habitat loss". 2011. Nature 473: 368-371. doi:10.1038/nature09985)</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">-----------------------------------------------------------------------------------</div><div style="font-family: Arial,Helvetica,sans-serif;">1. Yeah, I am aware I'm posting this a little late. So sue me.</div><ul style="font-family: Arial,Helvetica,sans-serif;"></ul>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-12232537179294808132011-05-21T19:30:00.001-06:002011-05-21T19:31:36.767-06:00Couldn't have said it better myself.<div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiaNjCuOUSn9ofxw1Y8PDIvuIbT1n2S3OpXhncaxJijHUABIWEJJ_o7LubuUzu1JcLQOFPh6qlFhV3m6zFH76XEjF5KtX2xOz76wGDWZt-NWZw6b2IUYEqxcgL26qQsouXiPXFSs2NfC6c/s1600/WQyPl.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="372" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiaNjCuOUSn9ofxw1Y8PDIvuIbT1n2S3OpXhncaxJijHUABIWEJJ_o7LubuUzu1JcLQOFPh6qlFhV3m6zFH76XEjF5KtX2xOz76wGDWZt-NWZw6b2IUYEqxcgL26qQsouXiPXFSs2NfC6c/s400/WQyPl.jpg" width="400" /> </a></div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: left;">Taken from <a href="http://lolscience.livejournal.com/72547.html">here</a>. </div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-45743873214223538682011-05-14T03:31:00.000-06:002011-05-14T03:31:12.768-06:00From Embryo to Adult: Body Plan Patterning in Drosophila - Part I<div style="font-family: Arial,Helvetica,sans-serif;">Take a look at a fly and it won't be long until you realize that even such a relatively simple creature is quite complex. This issue of complexity is a talking point for creationist rhetoric; "How can such complex structures just come together to create a fully formed individual?" they muse, "It must be the work of a divine creator!" Unfortunately for them, the process of development is well known and thoroughly understood. <a href="http://cwgk.blogspot.com/2011/05/from-embryo-to-adult-body-plan.html">In a series of posts,</a> I'll attempt to dispel this myth, and show just how a complex life form can arise from a single simple cell by entirely natural means. In this first part, I will introduce the concept of maternal effect genes, and one of the most important such gene, <i>bicoid</i>.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">The development from a single egg to a full adult fly is a long one, but the process begins long before fertilization ever occurs. Consider, for a moment, the process of fertilization in humans. In humans, the egg cell is monstrous in size compared to the relatively diminutive sperm cell. There is much more cytoplasm in an egg than in sperm, and that cytoplasm is full of mRNA, mitochondria and other cytoplasmic factors. These are ultimately donated to the embryo upon fertilization: the fertilized embryo contains nuclear genetic information from both parents, but contains cytoplasmic factors from the mother alone.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;"><i>Drosophila</i> are no different. The unfertilized egg is not just a storage container for nuclear DNA, but it contains mitochondria and mRNA which will ultimately become part of the embryo after fertilization. Many of those mRNA transcripts belong to a class of genes that is very important to the development of the body plan: <b>maternal effect genes<i>.</i></b></div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiMRD6IDQK97gzwm9n1YYllKNFI91PU2AKOgOKIUpIEED1K4Ny245TGnrYfsz9Cm9Tku-bHXE8voQ0vMZdTFWGRVPAoWP8tGodm5S7B9gS9cVAgSOn4fYkQYpwYJInkjPTTLkIwbLqNTus/s1600/drosophlia+embryo+fig+1.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="400" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiMRD6IDQK97gzwm9n1YYllKNFI91PU2AKOgOKIUpIEED1K4Ny245TGnrYfsz9Cm9Tku-bHXE8voQ0vMZdTFWGRVPAoWP8tGodm5S7B9gS9cVAgSOn4fYkQYpwYJInkjPTTLkIwbLqNTus/s400/drosophlia+embryo+fig+1.jpg" width="290" /></a>Maternal effect genes get their name from the fact that they are expressed in the mother, and not in the embryo. During oogenesis, the tissues in the ovary express these genes, and the transcripts are packaged into the embryo. This is in contrast to <i>zygotic</i> genes, which are expressed in the nuclei of the embryo itself. One thing that makes maternal effect genes so interesting is that individual females that are mutant in such genes are phenotypically normal: the phenotype shows up in the progeny instead<sup>1</sup>. There are about 50 maternal effect genes that play a role in the development of the <i>Drosophila</i> body plan, and they set up the basic framework for the zygotic genes that come later (which I will describe in a later part). Perhaps the biggest role they play, though, is in setting up the body plan axes.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">The <i>Drosophila</i> embryo has two axes: the anterior-posterior axis, and the dorsal-ventral axis (see <i>Figure 1</i>). If the the adult body plan is to be laid out in the developing embryo, it is important to make sure the embryo knows which side is which (you don't want the head to end up on the wrong end, for instance), and this is the primary goal for many maternal effect genes. The first of such genes that comes into play is called <i>bicoid</i>, and it works to determine the anterior-posterior axis of the egg. It does this through <b>morphogenic gradients<i>, </i></b>a concept that you'll see used extensively throughout development.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">Early on in the investigation of body plan development, it was noted that those mothers who are <i>bicoid</i> mutants give rise to progeny without properly differentiated anterior ends (they lack a head or thorax). This fact was interesting itself, but a series of experiments made the fact all the more striking. If you take an unfertilized <i>Drosophila</i> egg and poke the anterior end with a needle, allowing some of the cytoplasm to leak out, they end up developing into embryos that resemble those from <i>bicoid</i> mutants. Furthermore, if you were to transfer cytoplasm from the anterior end of a wild-type egg to the anterior end of a <i>bicoid </i>mutant egg, the embryos would develop normally<sup>2</sup>. It was also found that if the cytoplasm from the anterior end of a wild-type egg were transferred to the middle of a <i>bicoid</i> mutant egg, the embryos would develop a head right in the middle. This immediately suggested that there was some cytoplasmic factor in the anterior end of the egg that was lacking in <i>bicoid</i> mutant eggs, and this factor was responsible for establishing which end of the embryo became the anterior end.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjX9xRUPVFeztlXYyfWsdZlmz7tJnmbGiEJwbLdkW-qk_juKaGlyTp2zCy3d2PqbTsi6gXU6LcF0bLlIxrwGwQUDV4CsINw2VdyI9Q_2ac4v7KhQCBQAeNH9tr45CUiArr3bxyWRqERa6E/s1600/drosophlia+embryo+fig+2.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjX9xRUPVFeztlXYyfWsdZlmz7tJnmbGiEJwbLdkW-qk_juKaGlyTp2zCy3d2PqbTsi6gXU6LcF0bLlIxrwGwQUDV4CsINw2VdyI9Q_2ac4v7KhQCBQAeNH9tr45CUiArr3bxyWRqERa6E/s320/drosophlia+embryo+fig+2.jpg" width="252" /></a></div><div style="font-family: Arial,Helvetica,sans-serif;">If you were to look at the distribution of <i>bicoid</i> mRNA in the unfertilized egg, you would see just that (<i>Figure 2</i>). Before fertilization, <i>bicoid</i> mRNA is concentrated in anterior end. It remains untranslated until fertilization occurs. Upon fertilization, translation begins, and Bicoid protein diffuses through the embryo. Bicoid, then, forms a gradient, with high concentrations at the anterior end and low concentrations at the posterior end. Regions with a high concentration of Bicoid protein develop anterior structures, and the regions with a low concentration of Bicoid protein develop into posterior structures. The precise function of Bicoid will be explained in a later post, but for the moment, it is sufficient to know that bicoid activates particular zygotic genes in a concentration-dependant manner. Different zygotic genes have different threshold levels for activation, so the concentration of Bicoid across the embryo will determine which zygotic genes get activated, and in turn, determines what each region of the embryo develops into. This is the key principal behind a morphogenic gradient.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">But <i>bicoid</i> isn't the only maternal effect gene that plays a role in setting up the anterior-posterior axis. In the next part to this series, I will discuss three more important maternal effect genes: <i>nanos</i>, <i>caudal</i>, and <i>hunchback</i>.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;"><b><i>------------------------------------------------------------------------------------------------</i></b></div><div style="font-family: Arial,Helvetica,sans-serif;">1. If this seems confusing, remember that the genes are expressed in the mother, but the transcripts, and ultimately, the gene products, are packaged in the egg. If a maternal effect gene is mutated, the mother will be fine, but her progeny will not, because it is the eggs that are receiving the defective gene products.<b><i> </i></b></div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">2. This type of experiment is called a "rescue experiment", because it allows one to "rescue" the mutant embryos and allow them to develop normally.</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-52794169967511035982011-05-14T03:29:00.001-06:002011-05-14T03:31:43.249-06:00From Embryo to Adult: Body Plan Patterning in Drosophila<div style="font-family: Arial,Helvetica,sans-serif;">How a fully formed organism develops from a single fertilized egg cell is a complex process. That process is no less complex in inverterbrates than in verterbrates, and much is known about just how development occurs in <i>Drosophila</i>. In the following series of posts, I'll detail the just how you can get a complete fly from a simple cell.</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;">(Links will be available as I write and post each individual part)</div><div style="font-family: Arial,Helvetica,sans-serif;"><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;"><a href="http://cwgk.blogspot.com/2011/05/from-embryo-to-adult-body-plan_14.html">Part I: Setting up the Anterior - Posterior Axis : Bicoid</a></div><div style="font-family: Arial,Helvetica,sans-serif;">Part II: Setting up the Anterior - Posterior Axis: Hunchback, Nanos & Caudal</div><div style="font-family: Arial,Helvetica,sans-serif;">Part III: The Terminators</div><div style="font-family: Arial,Helvetica,sans-serif;">Part IV: Setting up the Dorsal-Ventral Axis: Spätzle, Toll and Dorsal</div><div style="font-family: Arial,Helvetica,sans-serif;">Part V: Zygotic Gene Expression along the D-V Axis</div><div style="font-family: Arial,Helvetica,sans-serif;">Part VI: Gap-gene Expression</div><div style="font-family: Arial,Helvetica,sans-serif;">Part VII: TBD</div>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0tag:blogger.com,1999:blog-1443345082398372535.post-23556944424831248962011-05-13T12:20:00.004-06:002011-05-13T12:23:49.537-06:00This Week in Science! (May 13, 2011)<span xmlns=""><span style="font-family: Arial,Helvetica,sans-serif;">This week has seen the publication of quite a few interesting research articles. Here is a list of some that have piqued my interest: </span><ul style="font-family: Arial,Helvetica,sans-serif;"><li><div><b>New Lizard Species Created in Lab</b> – Many species of lizards in the genus <i>Aspidoscelis</i> have an interesting life history. There are a dozen species of <i>Aspidoscelis</i> that live in New Mexico, and about half of these species reproduce by way of parthenogenesis. Among those parthenogenic species, some have triploid genomes (that is, they have three complete sets of chromosomes), while others are diploid (two sets of chromosomes). A team of researchers lead by Peter Baumann, however, has created a new species of <i>Aspidoscelis</i> – one that is tetraploid. Their paper, published in the <i>Proceedings of the National Academy of Sciences</i>, details how they crossed females of the species <i>Aspidoscelis exsanguis</i> – a parthenogenic triploid species – with sexually-reproducing diploid <i>Aspidoscelis inornata</i> males. The matings resulted in hybrid daughters that, upon karyotyping, were found to be tetraploid. These offspring went on to reproduce asexually, giving birth to daughters that were also tetraploid. This continued for multiple generations, effectively establishing multiple lineages of a brand new species! </div>(Baumann <i>et al</i>. "Laboratory synthesis of an independently reproducing vertebrate species". <i>Proc. Natl. Acad. Sci.</i>: doi/10.1073/pnas.1102811108) <span xmlns="http://www.w3.org/1999/xhtml"> </span></li>
</ul><ul style="font-family: Arial,Helvetica,sans-serif;"><li><div><b>Ribosomes Do More than Make Proteins</b> – Every biology student is taught that ribosomes are complex ribozymes that are the "protein factories" of the cell. But new research published in <i>Cell</i> indicates that ribosomes are actually involved in regulating genes as well. Maria Barna's team at UCSF took a look at <i>Ts</i>, <i>Tss</i> and <i>Rbt</i> mice – strains of mice that all have the similar phenotypes of short, kinked tails and an extra rib. These defects mapped to the distal region of Chromosome 11, and after cloning this region in <i>Ts</i> mice, they found that the <i>Rpl38</i> gene was deleted. Sequencing the region in <i>Tss </i>and <i>Rbt</i> mice showed similar problems in the <i>Rpl38</i> gene (a frameshift mutation due to a single nucleotide deletion, resulting in a stop codon and a truncated, nonfunctional protein in the case of <i>Tss</i> mice; and a dinucleotide insertion at the Intron 2/Exon 3 splice site, causing a frameshift leading to a truncated protein in <i>Rbt</i> mice). Ribosomes are complexes of nucleic acid and proteins, and RPL38 is one such protein. It was immediately obvious that RPL38 – and by extension, the ribosome - was involved in proper development of the body plan, a process controlled by Hox genes. One question remained: how? Interestingly, when they looked at the expression of the Hox genes, the transcript levels were unchanged, so RPL38 does not provide transcriptional regulation. Rather, they found that a subset of Hox gene transcripts was not being translated by the ribosome in <i>Rpl38</i> defective mice. In normal mice, RPL38 acts to facilitate the formation of the 80S ribosomal complex on these select Hox transcripts; in <i>Rpl38</i> defective mice, this does not occur, the Hox genes are not translated, and the mice are born with gross physical abnormalities. Looks like ribosomes just got a little bit cooler.</div>(Barna <i>et al</i>. "Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning". <i>Cell</i>: doi/10.1016/j.cell.2011.03.028)<span xmlns="http://www.w3.org/1999/xhtml"> </span></li>
</ul><ul style="font-family: Arial,Helvetica,sans-serif;"><li><div><b>Fascinating Fungi Find</b> – <i>Nature</i> this week published an article about an interesting mycological find that may have implications regarding the evolution of fungi. A team of researchers at the University of Exeter in the UK began by analyzing the genomes of microbes found in a local pond. Using the sequence data obtained from these samples, they constructed a phylogenic tree by comparing the sample data with that of known species of fungi. What they found was a set of unknown sequences that was basal to the known species. They then compared these unknown sequences to those obtained from samples collected in a large variety of environments, and discovered that the fungi were almost ubiquitous. Since they appeared to be found everywhere, but had not been previously discovered, the team named the fungi <i>cryptomycota</i> (or 'hidden fungi'). Intrigued, they designed fluorescently labeled DNA probes that were specific to cryptomycota DNA. This allowed them to visualize which cells in the sample belonged to their newly discovered fungi. They found that cryptomycota cells were very tiny (3-5 microns in diameter) ovoid in shape. But the truly interesting part was what they lacked: a cell wall made of chitin. A chitinous cell wall is considered the defining aspect of fungal species, so cryptomycota must represent a lineage that diverged very early on in fungal evolution. </div>(Jones, M. D. M. <i>et al</i>. "Discovery of novel intermediate forms redefines the fungal tree of life". <i>Nature</i>: doi:10.1038/nature09984) <span xmlns="http://www.w3.org/1999/xhtml"> </span></li>
</ul><ul><li><div style="font-family: Arial,Helvetica,sans-serif;"><b>Another Step Towards an HIV Vaccine</b> – also published in <i>Nature</i> this week is a report by Picker <i>et al</i> on a novel SIV vaccine. SIV (simian immunodeficiency virus) is a very close relative to HIV that infects monkeys. The researchers administered the vaccine – which consisted of SIV-antigen expressing cassettes inserted into a vector made from an avirulent cytomegalovirus – to a group of 24 rhesus monkeys. 59 weeks after immunization, the monkeys were given the SIV virus. When they monitored the infection in the monkeys, they found that 13 of the 24 showed continually diminishing viral loads, and by 52 weeks, the virus was rarely detected at all. Undoubtedly, it remains to be seen if the vaccine will remain effecting in preventing SIV infection over longer spans of time, but this development is nonetheless a groundbreaking step towards an effective vaccine for HIV.<b><br />
</b></div><span style="font-family: Arial,Helvetica,sans-serif;">(Picker </span><i style="font-family: Arial,Helvetica,sans-serif;">et al</i><span style="font-family: Arial,Helvetica,sans-serif;">. "Profound early control of highly pathogenic SIV by an effector memory T-cell vaccine". </span><i style="font-family: Arial,Helvetica,sans-serif;">Nature</i><span style="font-family: Arial,Helvetica,sans-serif;">: doi:10.1038/nature10003)</span><b><br />
</b></li>
</ul></span>C.W.G.Khttp://www.blogger.com/profile/16339226788815840900noreply@blogger.com0