HAVING been trumped last week by the decision of the chimpanzee genome-sequencing consortium to publish in their rival, Nature (see article), the editors of Science have now got somewhat of their own back with a trio of papers that look at genes which seem to be involved in the evolution of the human brain.
Two of these papers reported studies carried out by Bruce Lahn, of the University of Chicago, and his colleagues. Dr Lahn has been studying two genes that tell the brain what size to grow to. If either of these genes, known as Microcephalin and ASPM, fails to do its job properly, the result is a brain that, though normal in its structure, is far smaller than it ought to be—somewhere between a quarter and a third of the normal volume—and which does not work properly. One of the characteristics of Homo sapiens is an exceedingly large brain, and some biologists have speculated that changes in these two genes might be part of the cause of this enlargement. Those speculations have been supported by evidence that these genes have changed significantly since the human and ape lines separated several million years ago.
Dr Lahn has added to that evidence, and has shown that this evolution continued even after Homo sapiens became a species in its own right, less than 200,000 years ago. One variant of Microcephalin, now widespread, came into existence only about 37,000 years ago, while a widespread version of ASPM originated a mere 5,800 years ago—meaning that it post-dates the beginning of civilisation.
Dr Lahn and his team were able to estimate the dates that the two gene-variants first appeared by looking at which groups of people have them. The past two decades have revealed a lot about how humanity has spread across the globe, and when. By tracing branches of the family trees containing the variants in question backward until they join, the dates at which the variants appeared can be worked out.
That the two variants have spread by natural selection rather than chance can be seen from the speed with which they have become established. If they had no positive consequences, their frequency would rise, if at all, by chance—a process known as neutral drift.
The third paper, by Toshiyuki Hayakawa and Takashi Angata, of the University of California, San Diego and their colleagues, looks at a molecular receptor for a chemical called sialic acid. This chemical caused a stir a few years ago when it was discovered that human sialic acid is different from that found in apes—and, indeed, any other mammals. Dr Hayakawa and Dr Angata have found a receptor for sialic acid that occurs in human brain cells (though the cells in question are support cells rather than actual nerve cells), but not in those of apes. The gene that encodes this receptor molecule seems to have been cobbled together from bits of two other genes one of which, in a curious twist, had itself stopped working properly during the course of evolution.
What all this means is still mysterious. The study of brain evolution is still in the stamp-collecting phase that begins most branches of science, when researchers are looking for interesting facts to stick in their albums, rather than assembling overarching hypotheses. These three stamps, though, are very pretty. Eventually, they may turn out to be precious.