Dirac electrons broken to pieces

Abstract

This places their findings in harmony with previous results 9-11 that show FOXP2-related genes as evolutionary arbiters. Because the authors examine human-specific gene regulation by FOXP2, their work 3 may provide our first window on the co-evolution of regulatory networks that are important for human-specific features such as language, which probably require a number of genetic changes working in concert. So far, a variant of one FOXP2 target gene, CNTNAP2, has been associated 11 with heritable language impairment in children. Additional work is essential to elucidate the relationships between FOXP2 and the many other genes involved in these pathways. Konopka et al. 3 performed mass spectrom etry comparisons of FOXP2 chimp and FOXP2 human immunoprecipitates, but did not find major differences in the composition of associated proteins, which might have been expected if they interact with different transactivating factors. Furthermore, the region of the FOXP2 protein at which the two human-specific amino-acid changes occurred has an unknown function , leaving open the possibility that different DNA-binding characteristics might account for the observed disparities in gene expression. An alternative explanation for differential target-gene regulation by FOXP2 human and FOXP2 chimp may be the higher level of the human protein in the tested cells compared with the ancestral protein, perhaps owing to greater protein stability a larger pool of free FOXP2 might permit a relaxed DNA-binding specificity. However, because FOXP2 chimp causes greater changes in gene expression than FOXP2 human , such an alternative mechanism is less likely. Instead, the DNA that surrounds and includes the FOXP2-binding sites in the regulatory regions of target genes may provide a genomic context for their recognition by FOXP2 human. To explore this possibility, the authors 3 chose eight differentially expressed genes, and found that, for six of them, their short promoter regions exhibited differential activity that para-lleled the quantitative expression data. A careful analysis of those promoter DNA sequences may reveal common elements that result in dispa-rate activities with FOXP2 human and FOXP2 chimp. Co-evolution may likewise be important in the recognition sites, as similar sequences across the human genome may bear evidence of human-lineage-specific alteration. In summary, Konopka and colleagues' work 3 does what important discoveries usually do: it answers many questions, but raises even more. It confirms evolutionary relationships between FOXP2 proteins in different species revealed through genome sequencing, and uncovers potential mechanisms underlying the elaboration of human-specific traits such as speech. However, it also provides a starting point for future studies of the molecular basis of language and human evolution.