Science of Discworld III

related to mobile genetic elements known as group II introns, which are a ‘parasitic’ form of DNA that can invade host genomes and then remove themselves when the DNA is expressed as RNA. Moreover, they now seem to have a role as ‘signals’ in the regulation of genetic processes. An intron may be relatively short, compared to the long protein-coding sequences that arise when the introns are snipped out, but a short signal has advantages and can do quite a lot. In effect, the introns may be genetic ‘txt msgs’ in the mobile phone of life. Short, cheap, and very effective. An RNA-based ‘code’, running parallel to the DNA double helix, can affect the activity of the cell very directly. An RNA sequence can act as a very specific, well-defined signal, directing RNA molecules to their targets in RNA or DNA.
    The evidence for the existence of such a signalling system is reasonable, but not yet undeniable. If such a system does exist, it clearly has the potential to resolve many biological mysteries. A big puzzle about the human genome is that its 34,000 genes manage to encode over 100,000 proteins. Clearly ‘one gene one protein’ doesn’t work. A hidden RNA signalling system could make one gene produce several proteins, depending on what the accompanying RNA signal specified. Another puzzle is the complexity of eukaryotes, especially the Cambrian explosion of 525 million years ago, when the range of terrestrial body-plans suddenly diversified out of all recognition; indeed, was more diverse than it is now. Perhaps the hypothetical RNA signalling system started to take off at that time. And it’s widely known that the human and chimpanzee genomes are surprisingly similar (though the degree of similarity seems not to be 98 per cent as widely quoted even a few years ago). If our RNA signals are significantly different, that would be one way to explain why humans don’t greatly resemble chimps.
    At any rate, it very much looks as if all that ‘junk’ DNA in your genome is not junk at all. On the contrary, it may be a crucial part of what makes you human.
    This lesson is driven home by those business associates of parasitic wasps, the symbiotic polydnaviruses, sneakily buried inside the wasps’ own DNA. There is a message there about human evolution, and it’s a very strange one.
    Genome-sequencing may have been oversold as the answer to human diseases, but it’s very good basic science. The activities of the sequencers have revealed that wasps are not the only organisms to have bits of viral DNA hanging around in their genomes. In fact, most creatures do, humans included. The human genome even contains one complete viral genome, and only one, called ERV-3 ( E ndogenous R etro V irus). This may seem an evolutionary oddity, a bit of ‘junkDNA’ that really is junk … but, actually, without it none of us would be here. It plays the absolutely crucial role of preventing rejection of the fetus by the mother. Mother’s immune system ‘ought to’ recognise the tissue of a developing baby as ‘foreign’, and trigger actions that will get rid of it. By ‘ought to’ here we mean that this is what the immune system normally does for tissue that is not the mother’s own.
    Apparently, the ERV-3 protein closely resembles another one called p15E, which is part of a widespread defence system used by viruses to stop their hosts killing them off. The p15E protein stops lymphocytes, a key type of cell in the immune system, from responding to antigens, molecules that reveal the virus’s foreign nature. At some stage during mammalian evolution, this defence system was stolen from the viruses and used to stop the female placenta responding to antigens that reveal the foreign nature of the fetus’s father . Perhaps on the principle of being hung for a sheep as well as for a lamb, the human genome decided to go the whole hog 3 and steal the entire retroviral genome.
    When evolution carried out the theft, however, it did not just dump its booty into the human DNA sequence unchanged. It threw in a couple of introns, too, splitting ERV-3 into several separate pieces. It’s complete , but not connected. No matter: enzymes can easily snip out the introns when that bit of DNA is turned into protein. But no one knows why the introns are there. They might be an accidental intrusion. Or – pursuing the RNA interference idea – they might be much more significant. Those introns might be an important part of the genetic