FT247

Darwin’s On the Origin of Species was published 150 years ago. The idea of a “tree of life” had existed previously, but by introducing the idea of mutation Darwin showed how new twigs and branches formed. Every living thing would be assigned its place, and science would tidy up all the loose ends. In fact, the reverse happened. Molecular biology found snake genes in cows, algæ genes in sea slugs and a veritable legion of viruses incorporated into human genetic makeup. We are all, it seems, monstrous hybrids… what’s going on?

For a century after Darwin, the mechanism by which inherited traits were passed down remained a mystery. The blueprint for a creature existed somewhere in its cells, but many scientists assumed that the exact location would never be found. Then in 1953 the struct­ure of the DNA molecule was finally worked out (it had been discovered in the mid-19th cent­ury, before atomic or molecular structure were understood, and before many of the elements in the Periodic Table had been discovered) and scientists started to unlock its secrets – and found that you don’t just get DNA from your parents.

The passing of genes between species is known as horizontal (or lateral) gene transfer. The chief cause can be traced to viruses. A virus might be thought of as a piece of rogue genetic material that has gone into business on its own account. It takes over cells and causes them to start producing viruses. A small number of viruses – known as retroviruses – do this by overwriting the cell’s own DNA.

Viruses are also prone to mutations and copying errors. Researchers at the Tokyo Institute of Technology were therefore not too surprised to discover that the genome of the tatera­pox virus contains DNA from the carpet viper. At some point in history (thousands or millions of years ago) the virus infected a snake. A copying error meant that the virus picked up a section of (inert) snake DNA. Later on, the virus infected cattle; again a copying error meant that a section of inert virus DNA was left in the cattle genome. [1]
This can happen many times. A team at the University of Texas has found the same stretch of DNA replicated in mice, oposs­ums, anole lizards and clawed frogs. [2]

Retroviruses act as a natural genetic engineer, splicing genes from one species into another. Putting jellyfish genes into mice might be a monstrous thing to do – but it seems that nature has been doing this sort of thing for millions of years.

Although horizontal gene transfer can move genetic mater­ial from one animal to another, the most common result is to leave traces of virus in the host DNA. These remains are known as fossil or endogenous retroviruses, and there are a lot of them. Scientists studying the human genome have found a staggering 98,000 fragments of retrovirus, making up some eight per cent of the total. Most of your genetic heritage may be human, but you are one-twelfth virus.

It has always been assumed that these fossil retroviruses played no part in human develop­ment and that they were just “junk DNA” in the genome with no effect. However, recent research suggests that they may play a vital part in evolution. A retrovirus can cut and paste sect­ions of DNA; while this is usually destructive, sometimes the end result might benefit the host.

One of the key players in human genetics is a protein molecule called p53. It is not a gene, but a “master regulator” that switches genes on and off. Tim Wang of the University of California is a specialist in the new discipline of bioinformatics; he calls p53 “the most important molecule for humans”. It has been described as the guardian of the genome, as one of its most important roles is repairing the type of DNA damage that causes cancerous tumours. [3]

The p53 controller works by means of areas of DNA called “binding sites” – these are effect­ively the switches that it can turn on and off. Wang discovered that a third of the p53 binding sites are associated with stretches of fossil retrovirus. Two of the more important ones have been traced back to a period 40 million years ago, when primates were splitting into the two groups known as New World Monkeys and Old World Monkeys.

Rodents and other mammals that split from our lineage before then do not have the same p53 binding sites, and so are more vulnerable to some cancers. The evolutionary impact is still being debated, but it’s easy to see that we might never have become such a long-lived species without something like p53 to stop cancer from killing us all off at an early age.

Wangs’s team believe that the way that retroviruses cause changes in gene regulation and expression provides another type of evolution in addition to normal genetic mutation. If the extra binding sites are beneficial, then the carrier will thrive and pass them on to its offspring. Wang believes that future work will find that other master regulators besides p53 also work thanks to the intervention of ancient retroviruses. [4]  The tree of life always looked like a Victorian attempt to stack everything into a neat hierarchy; reality, as Fort could have predicted, is much more untidy. Darwin might have been happy to be the descendant of a monkey, but he might have been surprised to find he was cousin to a virus.

Notes
1 http://tinyurl.com/dyyr55 (New Scientist)
2 http://tinyurl.com/aky6hu (Proceedings of the National Academy of Sciences)
3 http://tinyurl.com/ywlyo4 (Cincinnati Children’s Hospital Medical Center)
4 http://tinyurl.com/bltu3m (Physorg.com science news)