In a study conducted by Dr.Erich Jarvis, it was discovered that mice have the capacity to regulate vocal communication just like humans. The gene of interest was the Forkhead box protein #2 (FOXP2) which regulates speech production in humans. Deficiencies in FOXP2 proteins leads to difficulty in formation of complex syllables and sentence structures. The study sought to determine whether FOXP2 deficiencies have similar consequences for communication in mice as they do in humans, supporting the “continuum hypothesis” that FOXP2 affects vocal production of all mammals.
The actual experiment featured 26 male mice heterozygous for the FOXP2 mutation and 24 “wildtype” male mice. The mice were placed in three social contexts: housed with an active wildtype female mouse, in proximity of only the urine of wildtype females, and housed with a sleeping female or male mouse. In the general case, healthy males produce different sequences and durations of ultrasonic vocalizations (high-pitched sounds). The results showed that the FOXP2 heterozygotes had difficulty producing the complex vocal communication patterns that wildtype mice can create with ease. Notably, in the social context with the active female mice, wildtype males were 3 times as likely as heterozygotes to produce the most complex syllable types and sequences reviewed.
A follow up study utilized transsynaptic tracing from vocal larynx muscles to compare the vocal brain regions of wildtype and heterozygote FOXP2 mice. It was revealed that the vocal motor neurons were more widely distributed across the cortex of heterozygotes than wildtype. This suggests that the FOXP2 mutation affects both the placement and functioning of the neurons connected to effective communication, for mice and humans.
As humans, we like to think that we are the top of the food chain, the most advanced of all species. This article helps minimize the circumference of our heads a little and proves that other mammals have in place the mechanisms for speech that enable us to communicate. I initially wondered why heterozygous FOXP2 where selected rather than homozygous. Further research revealed mice “homozygous for the mutationshowed severe motor abilities”. It was also interesting that the mice were placed in three different social contexts, in proximity only of the urine of female mice being the most bizarre of the three but probably equally effective for the experiment. Something that confused me was that deficiencies in the FOXP2 proteins have almost the same effect in humans as the presence of the mutation in mice. So, humans having less is bad but mice having simply the presence of FOXP2 is equally bad. The correlation is a bit fuzzy but even still, the experiment accomplished what it sought to: showed that FOXP2 influences the effectiveness of communication in both humans and mice.