In order to better understand the mechanism that resulted in the exon 7 amino acid substitution in humans and no other species, researchers compared the rate of protein sequence evolution in humans compared to that of chimpanzees. By obtaining protein sequences from different species and aligning them, using a rate analysis and computer simulations, they found that protein evolution rate in humans, compared to that of other primates, was significantly higher in human FOXP2 (Zhang et al. 2002). This provides a potential mechanism by which the FOXP2 gene evolved differently in humans. Although their analysis was thorough and insightful, other studies with different strategies that further confirm this potential mechanism …show more content…
The researchers discovered the same 2 amino acid substitutions in FOXP2 protein and proposed that the selective sweep identified in previous studies must have occurred between 300,000-400,000 years ago and originated in the common ancestor of Neanderthals and humans (Krause et al. 2007). This study is met with some resistance from other researchers, who propose that their conclusions on the timeline of the selective sweep are incorrect; they challenge the assumption that Krause made that the Neanderthals and humans did not interbreed at any point. Instead, they propose that the presence of the gene in both populations is a result of gene flow, a phenomenon where alleles or genes get transferred from population to population. They find that the previous authors may have also created assumptions about information that led them to ruling out contamination, which they feel may be premature and weakens the conclusion that Neanderthals carried the FOXP2 variants (Coop et al. 2008). This inconsistency in the literature hinders reaching a consensus about when the FOXP2 gene may have under gone the selective sweep. Further research would have to be done most likely on different bones from around that time …show more content…
The biggest unanswered question is whether this gene evolved in such a manner that it is the genetic basis of the evolutionary development of language neural circuitry. As discussed earlier, downstream targets of the transcription factor were identified, but there were only suggestions for the molecular pathways that were up and down regulated. Further analysis using comparison of the expression in FOXP2 to FOXP2chimp found specific accelerated highly conserved non-coding sequences in the human version and used whole-genome micro arrays to show the two amino acid mutations affect targets that are involved with the following: cerebellar motor function, craniofacial formation, and cartilage and connective tissue formation. This all heavily implicates human FOXP2 in the development of the neural circuitry and anatomical structures involved in language (Konopka et al. 2009). This study is great for further support that FOXP2’s implication in the development of language, but there remain questions about if it can be considered the sole genetic basis of the development of