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.
Opinion:
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.
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