Science writers typically have a few favourite stories: scientific detective stories or debates that intrigue at first encounter, then exert a siren call on the psyche for years, even decades, to come.

The story of Professor Emeritus Jack Pettigrew's quest to confirm that fruit bats (Megachiroptera) are flying cousins of primates has been a personal favourite since I first wrote about it in The Age the early 1990s. Both a detective story and a debate, it has twisted and turned for nearly 18 years, always intriguing, but without final resolution.

Pettigrew's story, which featured in the January/February edition of Australian Life Scientist, clearly appealed to our readers as well - it attracted the most comment of almost any article in recent times.

Just after ALS went to press, Pettigrew drew my attention to a new study, published in the open-access on-line journal, Public Library of Science 1 (PLoSOne), titled 'Accelerated FOXP2 Evolution in Echolocating Bats'.

The letters 'FOXP2' in the title leapt out of the page. The forkhead transcription factor gene FOXP2, known to some as the Chomsky Gene, has strong claims to the title of Most Interesting Gene in the Human Genome.

FOXP2 is active during early embryonic development in the developing gut, heart, lungs and, most significantly, in the brain. One of most highly conserved genes in vertebrates, it is essentially invariant among terrestrial vertebrates including reptiles, birds and mammals.

So a decade ago, when researchers learned that evolution had co-opted FOXP2 to a unique and remarkable role in the human brain, I was instantly intrigued - along with all those evolutionary geneticists sifting the human genome in search of the key genetic changes that made us so different from our higher primate cousins, chimpanzees, bonobos and gorillas.

Like most mammals, mice have the archetypal FOXP2, but in humans, three mutations have occurred in a particular exon of FOXP2 over the 80 million-odd years since the ancestors of mice and men parted evolutionary company.

My first encounter with the then-unidentifed FOXP2 gene was at a research conference at the Menzies Hotel in Melbourne in 1997. Professor Anthony Monaco, a UK Wellcome Trust researcher, gave a talk on his search for a mutant gene at a locus on chromosome 7, that he was calling Speech7. The mutation caused a severe speech disorder in three generations of the KE family.

In 1996 Monaco was hunting for genes involved in autism when clinicians at the Institute of Child Health in London drew his attention to a family in which three generations suffered from a severe inherited speech disorder.

The dominant mutation - it affected around 50 per cent of KE family members - disrupted the finely coordinated movements of the muscles, tongue and lower face required to speak intelligibly.

Further studies showed the mutation also affected areas of the brain involved in comprehending and producing grammatical speech - the "language engine" that US linguist Noam Chomsky theorised is hard-wired into the neural circuitry of the human brain.

Affected KE family members lack simple grammatical rules for spoken and written language, such as creating plurals from singular nouns or knowing that a person who builds is a "builder". They also perform poorly at language tasks, such as writing down a list of words beginning with the letter 'b'.

At the International Congress of Genetics in Melbourne, in 2003, US geneticist Molly Przeworska, from Svante Paabo's team at the Max Planck Institute for Evolutionary Anthropology in Germany, described her research to determine which human genes have been under the strongest selection pressure in the relatively recent past.

When a mutant allele arises that confers a major advantage in survival and reproduction, it will eventually dominate in a freely interbreeding population, at the expense of all other alleles. The phenomenon is called a selective sweep.

When a selective sweep occurs, genes flanking the new allele are also swept up and passed to the individual's descendants en bloc. In a relatively short period of time, the mutant allele and its time-travelling hangers-on dominate, driving rival linked alleles to extinction. A selective sweep effectively bleaches the locus of variation, so all individuals are invariant at that locus.

Over evolutionary time, the locus accumulates new, random mutations at a predictable rate, that allows the approximate timing of the selective sweep to be estimated.

Of the 112 candidate genes that Molly Przeworska compared for evidence of relatively recent selective sweeps, one gene on chromosome 7 emerged as almost white hot: FOXP2.