You can now read the Krause et al (2007) paper from Current Biology regarding the FOXP2 variant found in Neanderthals in an open-access on-line form at Current Biology Online. Here is the summary of the article:

Although many animals communicate vocally, no extant creature rivals modern humans in language ability. Therefore, knowing when and under what evolutionary pressures our capacity for language evolved is of great interest. Here, we find that our closest extinct relatives, the Neandertals, share with modern humans two evolutionary changes in FOXP2, a gene that has been implicated in the development of speech and language. We furthermore find that in Neandertals, these changes lie on the common modern human haplotype, which previously was shown to have been subject to a selective sweep. These results suggest that these genetic changes and the selective sweep predate the common ancestor (which existed about 300,000-400,000 years ago) of modern human and Neandertal populations. This is in contrast to more recent age estimates of the selective sweep based on extant human diversity data. Thus, these results illustrate the usefulness of retrieving direct genetic information from ancient remains for understanding recent human evolution.

The authors actually get more specific regarding the role of FOXP2 in language:

Although language and speech are clearly genetically complex phenomena, the only gene currently known that has a specific role in the development of language and speech is FOXP2. The inactivation of one FOXP2 copy leads primarily to deficits in orofacial movements and linguistic processing similar to those in individuals with adult-onset Broca’s aphasia

While the paper by Krause et al is an important contribution because it involves allele-level comparison of nucleic genetic material between hominid groups and across living and extinct forms, the role of FOXP2 and the characterization of the genetics of language may be misleading, if not simply very very wrong. Continue reading Framing the Language Gene: FOXP2 →