Human evolution


Three of a kind

Sep 8th 2005

From The Economist print edition


Some very human genes


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.