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Chimpanzees compared to humans
Chimpanzees were also found to have the FOXP2 gene, however the human version of the gene differs by a mutation change of two amino acids. A study was conducted at UCLA to test how this difference leads to only humans being capable of our language. The study found the FOXP2 gene mutation to be implicated in a developmental speech disorder that was transmitted through a family with an autosomal dominant inheritance pattern. A study in Germany sequenced FOXP2’s complementary DNA in Chimps and other species to compare it with human complementary DNA in order to find the specific changes in the sequence that have evolved through natural selection. FOXP2 was found to be functionally different in humans compared to chimps and this difference is said to account for the development of structures that allow the human capability of language which chimps lack. Since FOXP2 was also found to have an effect on other genes, its effects on other genes is also being studied. This mutation in the FOXP2 gene present in humans was also found in Neanderthals.

The human version of the gene differs from the chimp in their functions and in their appearance, due to the amino acid substitution that has evolved in the version that humans carry. Since FOXP2 is a transcription factor, it has been found to control other genes which are being studied in their functions in language development. Additionally, there were found different effects onto the targets of the FOXP2 gene in humans in how and whether there was expression of these additional genes. In this way, it is the FOXP2 gene’s functioning that allows humans to be able to have language but does not allow chimps this same ability. Researchers deduced that this finding could be used to further study other unique human abilities such as higher up cognitive functioning that chimps are not able to exhibit. There can also be further clinical applications in the direction of these studies in regards to illnesses that show effects on human language ability. [citation]

under mice section:

A study conducted at the Max-Planck Institute for Evolutionary Anthropology added the substitution of FOXP2 that occurs in humans into mice, and found this effects the basal ganglia in its circuits with cortical areas. They did this by transferring the human allele of the FOXP2 gene mutation into the mouse embryos through homologous recombination in order to create this model. Through testing these mice, they found that this mutation of the gene also had an effect on the exploratory behavior of the mice they were testing in lab. In comparison with how this gene mutation functions in humans, they found that in the mouse model it showed opposite effects when they were testing its effect on the levels of dopamine, plasticity of synapses, patterns of expression in the striatum and behavior that was exploratory in nature.

It was also found that when the FOXP2 gene was disturbed in mice, it effected many different processes in the mice including the learning motor skills and the plasticity of synapses. It makes sense for the gene to have a role in the processing of sensory inputs because of its effects in the cortical and subcortical regions of the brain such as in the olfactory bulb, auditory and visual circuits as well as in somatosensory regions of the thalamus. Additionally, FOXP2 is found more in the sixth layer of the cortex than in the fifth so this is consistent with it having greater roles in sensory integration. FOXP2 was also found in the medial geniculate nucleus of the mouse brain which is the processing area that auditory inputs must go through in the thalamus so it was found that its mutations play a role in delaying the development of language learning. It also makes sense for FOXP2 mutations to have roles in the learning, integrating and outputs of motor functions due to its high expression found in the Purkinje cells and cerebellar nuclei of the Cortico-cerebellar circuits. High FOXP2 expression has also been shown in the spiny neurons which express type 1 dopamine receptors in the striatum, substantia nigra, subthalamic nucleus and ventral tegmental area. The negative effects of the mutations of FOXP2 in these brain regions on motor abilities were shown in mice through tasks in lab studies. When analyzing the brain circuitry in these cases, scientists found greater levels of dopamine and decreased lengths of dendrites which caused defects in long term depression which is implicated in motor function learning and maintenance. Through EEG studies, it was also found that these mice had increased levels of activity in their striatum which contribute to these results.

There is also evidence for mutations of targets of the FOXP2 gene shown to have roles in schizophrenia, epilepsy, autism, bipolar and intellectual disabilities. [citation: French et. al.]