Monday 3 May 2010

You are descended from Viruses, not Apes

The blog title is a cheeky play on a chapter in the Matt Ridley book, Genome, which compares the fact that our genome has more genes of useless viral origin than genes which actually code for something useful: only 4% of the human genome actually do something (99% of which is the same as our closest relatives, the chimpazees), while a whopping 21% is composed of self-propagating remnants from retrograde viruses (e.g., LINEs, see Griffiths Introduction to genetic analysis 2009). We’ve been hijacked. Does this make you feel incredulous, or give you a sense of awe? No doubt it does, so long as you adhere to the illusion that you are some cohesive whole, and that “your” genes exist solely for your benefit. A view more in line with the facts, however, is that the “I” is just the accidental ambassador for a troublesome nation of genes.

I like this fact as a way to set the context for two paradigm-smashing themes in evolution and genetics, namely, a) our genome is a demonstrably flawed “set of instructions” (if viewed through the lens of a “Designer”), and b) We, or rather, “I”, the seemingly unified human individual, is merely a vehicle for the selfish propagation of many genes, among them with great schisms and outright war, competing to do what they exist only to do: getting themselves duplicated.

Consider the most common protein gene in the human genome, Reverse Transcriptase gene, which has no useful application for us or our cellular machinery, but is employed by retroviruses such as HIV. Reverse Transcriptase takes RNA (say, from a virus), transcribes it into DNA, wherein other enzymes can inserts it into our genome. Why do we have a gene that does nothing else but potentially insert viral RNA into our genome? Other genes have done away altogether with their viral middleman, such as Retro-Transposons, and do nothing but replicate themselves with Reverse Transcriptase.

(See a video on Reverse Transcriptase and HIV)

These facts, and others, such as 96% of the human genome being “junk DNA”, challenge all attempts to “make common sense” of the genome. Forget all the info/media analogies you’ve heard about the genome, such as it being like a blueprint, a recipe, an instruction manual, or a program for proteins. The genome is absurdly far from being a coherently “authored” document. For example, an analogous “Instructions Manual For How to Build a Protein”, would make Pulitzer Prize-winners of the most hopefully convoluted IKEA Instruction Manuals in comparison:

“At least [Instruction Manuals] do not insert… five copies of the Schiller’s Ode to Joy, or a gargled version of a set of instructions for how to saddle a horse. Nor do they generally include five copies of a complete set of instructions for how to build a machine that would copy out just that set of instructions. Nor do they break the actual instructions you seek into twenty-seven different paragraphs interspersed with long pages of irrelevant junk, so that even finding the right set of instructions is a massive task. Yet, that is a description of the human Retinoblastoma gene, and as far as we know, it is typical of human genes: 27 brief paragraphs of sense, interrupted by 26 long pages of something else”(Matt Ridley, in Genome).

This is because our genome is a document which wrote itself, rather being Authored, Designed, or Created. And (to extend the absurd analogy) rather than the whole document having its own interest at heart, individual paragraphs are clamouring and competing for selfish verbosity.

Some genes increase themselves in the greater gene-pool by genuinely improving their hosts’ chances of staying alive and reproducing, such as genes which code for language or blood-clotting. Other’s do it by hijacking our DNA-replication machinery.

The point is that the focus of evolution is not at the species-level, nor even at the individual-level, but at the level of the gene. Just like it is wrong to say that natural selection promotes traits which benefit the species (consider 2-tonne male Elephant Seals pulverizing young pups – even their own – in their frantic race to rape females), so too does natural selection sometimes promote genes which are bad for the individuals who harbour them (but are good at getting the gene’s replicated more, so all the better).

How to think of this gene-level view of evolution and natural selection? One way is to build family trees for each individual gene. As an organism, you have a unique family tree which branches backwards in time with 2 parents, 4 grandparents, 8 great-grand-parents, 16 great great-grand-parents, and so on, all of which, more or less, contributed a corresponding proportion of their genome to you. However, each individual gene has a different story: each copy came from only 1 parent, 1 grand-parent, 1-great-grand-parent, and so on ad infinitum. This difference between genetic lineage and ancestry is key to understanding evolution. For example, we may have genes whose origins do not show up at all in the parental ancestry, such as from viruses. Likewise, we may have ancestors who contribute next to nothing of our genome, but nonetheless mated with one of our great-, great-, great- … grand-mothers. For example, African Homo sapiens likely interbred with European Neanderthals passing on hybrid-children, but the children with proportionally more H. sapiens genes were favoured by natural selection, until the exo-species genes were culled away. (This is one way to reconcile the seemingly contradictory evidence for an “Out-of-Africa” hypothesis that all homo sapiens are descended from Africa, and the Multi-Regional hypothesis, that Homo sapiens evolved from different Homo erectus variants already in different parts of the globe. Nearly all of our genes have a family-tree that traces them back to the march of H. sapiens spreading out of Africa. But, some people have features which seem to come from Neanderthals, such as the mysterious bridged-form of the mandibular nerve canal, present in 6% of Europeans today, but no where else. Very little else of the neanderthals’ genes survived.)

In future blogs, I’ll discuss how this flawed genome with its various competing genes can explain many mysteries of the human experience.

See Genome by Matt Ridley.

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