Addition of Genetic Information Made Simple

A common argument among creationist types is that evolution is impossible because it requires an addition of genetic information to a genome, which, they say, never happens. Instead they posit that genetic information is only ever lost through mutation A mutation in a gene encoding for alcohol dehydrogenase, for instance, results in the loss of the ability to metabolize alcohol. This represents a loss of genetic information. Further, they claim that beneficial mutations are exceedingly rare (or impossible) - a claim that is incredibly fallacious - and because of this, evolution is impossible. Some creationists have even claimed that this question stumped Richard Dawkins himself, however this has been shown to be an outright hoax.

The most obvious problem with this claim is that what is meant by "information" is never actually defined by creationists. Do they mean new genetic "instructions" - new and different genes being added to a genome? Do they mean new physical DNA being added to expand a genome? "Information" is quite a vague term, and can mean a multitude of things.

I would assume, however, in most cases, "information" refers to new genes being "added" to a genome, since genes ultimately supply the "information" or "instructions" an organism needs for body plan organization, carrying out metabolic processes, growth and development. And if the claim really is that there are never new genes added to a genome, then the claim is blatantly false.

Adding new "information" to the genome is actually quite simple and very common in the natural world (that is, outside the laboratory). It's a little process called gene duplication.

I won't get into all the nitty gritty details about the various ways that gene duplication occurs, because they're not all that relevant to the topic at hand, but common causes of gene duplication are homologous recombination, retrotransposition, or simply errors in DNA replication (the DNA Polymerase slipping back along the DNA strand, for instance). In either instance, the result is an extra copy of a gene is present in the genome.

A great example of gene duplication are the human globin genes. We do not simply have one gene for "hemoglobin"; rather, humans have a variety of hemoglobin genes: α-hemoglobin, and β-hemoglobin are the two expressed the most in adults, with ε- and ζ-hemoglobin expressed in the embryo, and γ-hemoglobin expressed during all stages of development. It should be of no surprise that all of the hemoglobin genes, despite being expressed at different times during the human life cycle and having slightly different functions, are all very related. The various forms of hemoglobin have arisen through gene duplications. According to Ross Hardison¹,

"In the distant past, some ancestral - probably single-celled - organism had one hemoglobin gene, and therefore one kind of hemoglobin protein. But at some point, this gene was duplicated, so that each of the resulting daughter cells carried two identical copies of the ancestral hemoglobin gene. Gradually, during successive cell divisions, small variations in the sequence of nucleotides - the subunits that make up a gene - started to appear. In this way, the two genes that started out identical acquired sequence differences and later, functional differences. It is quite likely that additional hemoglobin genes were acquired the same way, by gene duplication followed by modifications in the nucleotide sequence."

I can already hear the cries of the creationists. "But," they proclaim, "this doesn't show evolution at all, for the different hemoglobin genes are still all the same kind!" (Oh how I hate that dreaded "kind" word). This is where gene duplications can get interesting. Once a gene duplication occurs, you have an extra copy of whatever gene that's been duplicated in your genome. This essentially works like a "backup" copy of the gene. Since a lot of mutations are deleterious (but not most mutations, as the creationists would have you believe), then having this backup copy gives a clear advantage - one copy is free to be mutated without the organism encountering any deleterious effects. These duplicated genes gain mutations at a faster rather than other genes, since potentially disastrous mutations in them won't kill the organism, allowing them to be passed on to future generations and sustain even more mutations (compared to a non-duplicated gene, where a disastrous mutation kills the organism, so neutrally and unmutated copies are what get passed on to future generations).

What does this mean? It means that the gene now has the potential to take on new functions, different regulation, etc. In essence, the duplicated copy has the potential to become an entirely new gene - one that gives an entirely new function - such as being able to metabolise a new food substrate, break down toxic compounds or grow larger and more quickly. New genetic "information" has been added to the genome.

It amazes me that the "no new genetic info" claim is still such a common one among creationists. Gene duplication as a major player driving evolution has been accepted by the scientific community for the better part of the last 100 years². Indeed, Susumu Ohno had claimed back in 1967 that gene duplication is the single most important factor in evolution³. The reality is that new genetic "information" is added to genomes - yours, mine, every living organism's - quite easily and quite commonly.

EDIT: And it can get even easier. Prokaryotic organisms, like bacteria (and even some eukaryotes like amoeba) can take up bits of exogenous DNA (that is, DNA that is simply floating around in their environment), adding "new information" to their repertoire almost instantly!

EDIT #2: Looks as if some simple multicellular organisms like bdelloid rotifers are also able to take up foreign DNA from their environment.

------------------------------------
1. Hardison, R. (1999) . "The Evolution of Hemoglobin" American Scientist 87.2: p126
2. Taylor, JS. & Raes, J. (2004). "Duplication and Divergence: The Evolution of New Genes and Old Ideas" Annual Review of Genetics 9: 615-643
3. Ohno S. 1967. Sex Chromosomes and Sex-linked Genes. Berlin: Springler-Verlag. 192 pp.

Fancy new Header

I made a shiny new header for my blog. It's more eye-catching than the standard one that Blogger adds to your blog, but I still think it could be fancier. Think of it more as a pretty placeholder until I really whip out my Photoshop skills.

I was sure I swore more than this...

Seems my Cuss-O-Meter is registering as low. Only 1.7% of my pages contain cursing? I have a little more than 100 posts, meaning I've only swore in about two of them? I'm much more foul mouthed than that in real life...

Now to try and find a Blaspheme-o-Meter. That one'll probably have a thermonuclear meltdown analyzing my blog...

A Quick Primer to Kantian Philosophy

Immanuel Kant is a pretty important philosopher, but to laymen, his ideas aren't all that easy to understand. So here's a quick primer to his work that I swiped from Ron's Philosophy Page entitled Kant's Ethics: The Short Version:

• How would you like it if everybody did that?
• If you do something because you're a dick, but then it works out okay anyway, you're still a dick.

And that's pretty much it. Kantian morality is based around two ideas. First, the principal of universalization ("Act only according to maxims which you can will also to be universal laws", according to Kant). What this means is "only do things that work out well if everybody did them". Being honest works well if everyone does it, so according to Kant, being honest is moral. On the contrary, stealing doesn't work well if everyone does it, nor does lying. So according to Kant, these are not moral things to do.

Secondly, Kant believes that you should not use people as a means to achieve an end. In other words, if you do something immoral, even if the end result is something good, then it was still an immoral act.

If you'd like to learn more about Kant's views on ethics, I suggest picking up The Great Philosophers, by Stephen Law. It does a good job at exploring Kantian ethics in some detail, without getting too technical (as well as explain the philosophies of 49 other great thinkers). Highly recommended book!

Ann Coulter: Still Running off at the mouth, still doesn't have a clue.

I really hate Ann Coulter.
She has a long history of being a complete moron, including thinking Canada supported the US in Vietnam, claiming that Jews want to be "perfected", and storming out of an interview when she doesn't get her way.

I have yet to read any of her books (and for good reason, I would rather my brain not spontaneously combust), but this excerpt from her book Godless: The Church of Liberalism, is enough to prove that it's complete drivel. This is her take on the theory of evolution:

"Throw in enough words like imagine, perhaps, and might have -- and you've got yourself a scientific theory! How about this: Imagine a giant raccoon passed gas and perhaps the resulting gas might have created the vast variety of life we see on Earth. And if you don't accept the giant raccoon flatulence theory for the origin of life, you must be a fundamentalist Christian nut who believes the Earth is flat. That's basically how the argument for evolution goes."

No, Ann. That's basically how the argument for creationism goes. There is no definitive proof of a creator, much less of the Christian god; no proof of instantaneous creation of even a speck of dust, much less all the matter and energy in the universe; and no proof that any of the Biblical tale of creation is true. We are left to imagine that God exists, and decided on a whim that perhaps he should create a vast, mostly empty universe to house his most important creation - mankind - on a rock in the middle of galactic nowhere, and he might have done it by sneezing into a mud puddle.

While there are uncertainties in how life began (that's abiogenesis, Ann, not evolution), the theory of evolution is not just some story scientists came up with one day over tea and crumpets. It's the end product of two centuries (and indeed, even longer) of scientific work. Sure, there are things we don't know yet, but there is no imagining involved. We are lead to evolution by considering the evidence, and what the evidence presents to us factual.

I would imagine that perhaps Coulter should shut her skeletal maw, because she's so dense, her brain might have become a singularity. That's much more plausible than creationism, anyway.

Gene of the Week: FOXP2

The Gene of the Week is a new feature that I've decided to bring to my blog. Each weekend I'll (try to) write a bit about a gene and it's related gene product that I think is pretty cool.

This week's gene is FOXP2, a gene that has been implicated as having a role in the development of language skills, and is likely to have played a major role in shaping the early evolution of Homo sapiens.

FOXP2 is a member of the Forkhead Box gene family (called "forkhead" after the prominent helix-turn-helix motif that resembles a forked head). It's located (in humans) on the q-arm of chromosome 7, and has a 2285bp transcript. It's gene product, the FOX P2 protein, is fairly large, at 715 amino acids in length. The gene is required for the proper development of the brain and the lungs, but where the gene shines is it's involvement with speech and related processes.

The history of the gene is actually quite interesting. Around 1990, a family known simply as the KE family, caught the scientific community's attention. The family was of particular interest because, over the previous three generations, around half of the family members developed severe problems with speaking - to a point that their speech was quite incomprehensible and they had to rely on sign language to communicate - as well as other physical and mental handicaps. A pedigree of the family and the disorder showed a pattern of inheritance suggestive of a mutation in a single, autosomal dominant gene.

It was not until 1998, when Fisher et al.¹ did a linkage study and narrowed the location of the gene to a small region of chromosome 7 (7q31), and named the hypothetical gene SPCH1. Three years later, in 2001, Lai et al.² made an interesting discovery. Working with a patient that exhibited a similar to that of the KE family, they discovered that the patient had a chromosomeal translocation affecting chromosome 7. In fact, the break point of the translocation was in the very region that Fisher and colleagues pinpointed in 1998. Going back to the KE family, the team found that the same gene that was broken in their patient had a point mutation in all of the affected members of the KE family and was not found in any of the unaffected members or control groups. In effect, they had found the gene that was causing the disorder in the KE family. The popular media caught wind of this discovery and, unsurprisingly, overexaggerated the finding with claims of a "gene for language", implying that this was a gene unique to humans that allowed us to talk - a claim that was blatantly false.

The gene that Lai and fellows found was a member of the FOX gene family - FOXP2.

Since then, lots of work has been done on the FOXP2 gene. It's been shown to affect vocalization in mice pups, song learning in finches, and even in the development of echo-location in bats. It has also been found that the gene is widely conserved, from fish to alligators to humans. However, what makes the gene particularly interesting from an evolutionary standpoint is that the human form of the gene is a bit different from the rest: it differs from the form of the gene found in other primates by two amino acids. It is speculated by some researchers that this difference is what lead to the development of language in humans, though a mechanism for this is yet unknown. Other researchers are of a different mind, claiming that the two amino acid difference is unlikely to have resulted in the development of language, but rather, a difference in gene regulation - when and where the human form of FOXP2 is expressed - is a more likely origin.

Much work remains to be done on FOXP2. It is a known transcription factor, but the genes it regulated are still unknown. Investigations into its role in evolution will undoubtedly continue. Be sure to keep your eye out for developments in this gene; it's bound to shed some light on the recent evolution of our species.

-----------------------------------------------------------------
1. Fisher et al, Nat Genet 18, 168 –170 (1998)
2. Lai et al, 'A forkhead-domain gene is mutated in a severe speech and language disorder' Nature 413, 519 - 523 (2001)

For further reading and more details, see:
http://www.evolutionpages.com/FOXP2_language.htm
http://en.wikipedia.org/wiki/FOXP2
http://www.genenames.org/data/hgnc_data.php?match=FOXP2
http://www.wikigenes.org/e/gene/e/93986.html
http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nuccore&id=219518945

Atheism. Srsly.

Via Terahertz via Friendly Atheist:

How serious do you take your atheism?

Let’s find out.

Copy and paste the list below on your own site, boldfacing the things you’ve done. (Feel free to add your own elaboration and commentary to each item!)

1. Participated in the Blasphemy Challenge.
   
2. Met at least one of the “Four Horsemen” (Richard Dawkins, Daniel Dennett, Christopher Hitchens, Sam Harris) in person.
3. Created an atheist blog.
   
4. Used the Flying Spaghetti Monster in a religious debate with someone.
5. Gotten offended when someone called you an agnostic.
6. Been unable to watch Growing Pains reruns because of Kirk Cameron.
7. Own more Bibles than most Christians you know.
8. Have at least one Bible with your personal annotations regarding contradictions, disturbing parts, etc.
9. Have come out as an atheist to your family.
10. Attended a campus or off-campus atheist gathering.
11. Are a member of an organized atheist/Humanist/etc. organization.
12. Had a Humanist wedding ceremony
13. Donated money to an atheist organization.
    
14. Have a bookshelf dedicated solely to Richard Dawkins. (Not really, but I do own books by him OTHER than The God Delusion)
    
15. Lost the friendship of someone you know because of your non-theism.
16. Tried to argue or have a discussion with someone who stopped you on the street to proselytize.
17. Hid your atheist beliefs on a first date because you didn’t want to scare him/her away.
18. Own a stockpile of atheist paraphernalia (bumper stickers, buttons, shirts, etc).
19. Attended a protest that involved religion
20. Attended an atheist conference.
    
21. Subscribe to Pat Condell’s YouTube channel
22. Started an atheist group in your area or school.
23. Successfully “de-converted” someone to atheism.
24. Have already made plans to donate your body to science after you die. (Considering it)
    
25. Told someone you’re an atheist only because you wanted to see the person’s reaction.
26. Had to think twice before screaming “Oh God!” during sex. Or you said something else in its place.
27. Lost a job because of your atheism.
28. Formed a bond with someone specifically because of your mutual atheism (meeting this person at a local gathering or conference doesn’t count). (There are lots of reasons Jess and I got along so well when we met but both of us being atheists was a major one)
    
29. Have crossed “In God We Trust” off of — or put a pro-church-state-separation stamp on — dollar bills.
30. Refused to recite the Pledge of Allegiance. (Or Canadian national anthem)
31. Said “Gesundheit!” (or nothing at all) after someone sneezed because you didn’t want to say “Bless you!”
32. Have ever chosen not to clasp your hands together out of fear someone might think you’re praying.
33. Have turned on Christian TV because you need something entertaining to watch
34. Are a 2^nd or 3^rd (or more) generation atheist.
35. Have “atheism” listed on your Facebook or dating profile — and not a euphemistic variant.
36. Attended an atheist’s funeral (i.e. a non-religious service).
37. Subscribe to an freethought magazine (e.g. Free Inquiry, Skeptic) (Nope, but I usually pick up a copy of Skeptical Inquirer when Im at Chapters)
38. Have been interviewed by a reporter because of your atheism.
39. Written a letter-to-the-editor about an issue related to your non-belief in God.
40. Gave a friend or acquaintance a New Atheist book as a gift.
41. Wear pro-atheist clothing in public.
42. Have invited Mormons/Jehovah’s Witnesses into your house specifically because you wanted to argue with them.
43. Have been physically threatened (or beaten up) because you didn’t believe in God.
44. Receive Google Alerts on “atheism” (or variants). (Not anymore though)
45. Received fewer Christmas presents than expected because people assumed you didn’t celebrate it.
46. Visited The Creation Museum or saw Ben Stein’s Expelled just so you could keep tabs on the “enemy.”
47. Refuse to tell anyone what your “sign” is… because it doesn’t matter at all.
48. Are on a mailing list for a Christian organization just so you can see what they’re up to…
49. Have kept your eyes open while you watched others around you pray.
50. Avoid even Unitarian churches because they’re too close to religion for you.

And the scoring system:
0-10: Impressive, but not too far from agnosticism.
11-20: You are, literally, a “New Atheist.” But you now have something to strive for! Go for the full 50!
21-30: You are an atheist, but babies aren’t running away from you. Yet.
31-40: You are the 5^th Horseman! Congratulations!
41-50: PZ Myers will now be taking lessons from you

Relativity explained in four letter words.

Ever wanted to try and understand relativity but just couldn't get your head around the complicated terminology and somewhat abstract thinking? Then this is for you:

Short Words to Explain Relativity

Brian Raiter has written up a great explanation of relativity, and to the delight of laymen out there, it's written entirely in words that contain four letters or less.

It's a great read. So what are you waiting for? Go read it!

You think I can get this on a shirt?

Taken from Komplexify:

Botox: If they only knew...

Humans are vain creatures. Perhaps only cats can tie humans on the vanity scale. And because we're so vain, we (or at least a select demographic) have become accustomed to poking, prodding, nipping, tucking, and injecting to make ourselves look younger and more beautiful. I'm talking, of course, about cosmetic surgery. It's reported that in the U.S alone, 11 million cosmetic surgeries were done in 2006. It's hardly a small industry.

But of all the different procedures which have become commonplace in the world of cosmetic augmentation, one has become particularly popular in the recent years: Botox.

Botox is a treatment used to get rid of unwanted wrinkles. Supposedly, it works well, because I doubt it would be so popular if it didn't. But there is one important fact about Botox that I don't believe many people who undergo the treatments ever ask themselves: what, exactly, is Botox?

To answer that, first we have to take a look at the lovely bacterium Clostridium botulinum (see the lovely image to the right), or rather what C. botulinum is best known for: it's toxin. If you or your parents or grandparents have ever made canned or jarred preserves, or if you have ever bought any from a farmer's market, then you are probably familiar with one big danger of eating such foods - botulism. If canned/jarred foods are not prepared correctly, you run the risk of contamination by C. botulinum. When ingested, the bacterium produce a toxin known as botulinum toxin, leading to botulism. Botulism is no simple food poisoning, either. Botulism is deadly. It causes a paralysis of the muscles and is very often deadly. It's so deadly that a 12oz glass of botulinum toxin is enough to kill every single person on the planet.

To understand the mechanism by which botulinum toxin (BTX) works, I should first explain a bit about how neurons work. When a signal is transferred from one neuron to another, it relies on the function of a neurotransmitter called acetlycholine (ACh). In general (and this is pretty general; I won't go into action potential polarization/depolarization), when an impulse travels down the axon of a neuron, it allows for ACh to be released across the synapse (the synapse is the space between the axon of one neuron and where it touches another). When the ACh reaches the surface of the next neuron, it binds to cellular receptors which signal to the neuron to continue the impulse, and the process continues from neuron to neuron. The whole process hinges on ACh being released and passed on to the next neuron down the line.

Inside of a neuron, ACh is stored in "synaptic vesicles". Think of them as little membrane-bound spheres that hold ACh until it's needed. In order for the ACh to go from inside the synaptic vesicle to the outside of the neuron, the vesicles bind and fuse to the axon membrane, releasing the ACh into the synapse. This process of binding and fusing is facilitated by two key proteins: synaptobrevin and SNAP-25. Synaptobrevin is a VAMP, or Vesicle-Associated Membrane Protein. In other words, Synaptobrevin sits on the outside of the synaptic vesicle. SNAP-25 sits on the cytoplasmic face of the axonal membrane. These two proteins interact with each other; synaptobrevin latches on to SNAP-25 to form what's known as a SNARE complex. The formation of this complex is what allows the synaptic vesicle to bind and fuse with the cellular membrane.

If all of that confused you, then let me put it in simpler terms. Synaptobrevin on the vesicle anchors onto SNAP-25 in the axon, allowing the vesicle to attach to the cellular membrane. The two fuse and ACh is released into the synapse. The nerve impulse is allowed to continue.

This is where botulinium toxin comes in. The BTX toxin is actually a protein consisting of two chains: the light chain and the heavy chain. The heavy chain is responsible for getting BTX into neurons; it binds to structures on the surface of the neuron, whereby it is internalized by endocytosis. Next, it's the light chain's turn to do it's dirty work. The light chain of the toxin actually works as a protease (that is, it cleaves proteins). The protein of choice of the light chain actually depends on the type of BTX toxin in question. BTX-A will cleave SNAP-25, whereas BTX-B will cleave synaptobrevin. Either way, the consequence should be obvious. With one of the components of the SNARE complex missing, the synaptic vesicles cannot bind and fuse, and ACh can no longer be released into the synapse.

This is bad news. With ACh being trapped inside of the neurons, neuronal impulses cannot be sent from one neuron to the next. This means that you can no longer send signals to your muscles telling them to relax or contract. You become completely paralyzed.

But what does all of this have to do with Botox, you ask? Well, Botox is simply a brand name for none other than botulinum toxin. It's actually botulinum toxin that cosmetic surgeons inject into your skin to make those wrinkles disappear. Wrinkles are caused by overactive muscles, and by injecting Botox, one can force them to relax and *poof*, no more wrinkles.

It is perfectly safe: the amount of toxin used is very small, and poses no significant health risks.
Nevertheless, I can't help but think that the popularity of Botox treatments would be on the rapid decline if more people knew that they were actually injecting the world's most toxin protein into their faces.