Mice with a human "speech gene" squeaked in a bass voice
The speech gene did not make the mice talkPyotr Smirnov, "Newspaper.
Ru»Despite the various tricks that laboratory mice can do, scientists are still trying to expand the arsenal of tricks of their wards.
Super–tolerant, super-strong, ultra-fast, super-resistant or, conversely, super-susceptible to the most dangerous diseases - the list of genetically acquired abilities by the will of scientists is not limited to this.
Wolfgang Enard of the Max Planck Institute for Evolutionary Anthropology in Leipzig and his colleagues have set themselves an almost insoluble task – to teach mice to speak. Well, or at least transplant the human version of the Foxp2 speech gene to mice.
Mice, and other animals, including primates, also have this gene, or rather, the DNA sequence encoding the transcription factor Foxp2, but differs from human by two point mutations. It is believed that these mutations gave a person a unique ability to both speak and distinguish speech. Scientists differ in the estimates of the age of this mutation – from 100 to 500 thousand years. The question of the age and evolution of Foxp2 has even become almost the main topic in the discussion of the recently decoded genome of Neanderthals.
However, the effects of this transcription factor are still unclear. Obviously, such a complex process as speech cannot be provided by just one gene, an appropriate structure of the respiratory tract and vocal cords is necessary. In addition, the brain and the hearing organ should be able to perceive and distinguish this very speech. Foxp2 is the best fit for the role of a "regulator" – after all, it is a transcription factor that regulates the work of a wide variety of genes (which ones are not fully known). That is, one mutation in the Foxp2 gene is enough to change the structure, properties and functions simultaneously in several tissues – be it the nervous or respiratory system.
Foxp2 became the "speech gene" relatively recently: at the end of the last century, it turned out that its mutations are the cause of congenital defects in speech perception. But the mechanism of action, as well as all the functions of this factor, remained unknown until today. Looking ahead, let's say that even after Enard's work, many questions remained, although scientists managed to describe the effects of the human version of Foxp2 on mice. The authors of the Cell publication, whose enumeration together with the institutes took up the entire first page of the article, tried to answer two questions at once: what is the role of Foxp2 in general and what is the difference between the effects of human Foxp2 and mouse.
To do this, they first had to breed mice heterozygous for this gene – Foxp2wt/ko (wild type/knockout), that is, one variant of this gene was "wild" – mouse, and the second was turned off completely. In addition to this group, the scientists also obtained Foxp2hum/hum (human) mice, which had a human variant of the gene in both positions. After that, Enard and colleagues, among whom was Svante Peebo, the "chief expert" on the Neanderthal genome, evaluated the mice according to almost three hundred physiological criteria.
The "humanized" mice never learned to speak and even had less dopamine secretion and faded research enthusiasm, but they produced quantitatively different ultrasounds.
The absence of one copy of the gene led to an absolutely opposite effect, which once again proves the role of the human version of Foxp2 in all observed phenomena. The reason for these differences is in the basal nuclei of the terminal brain. It is here that signals are redirected from the cerebral cortex to the muscles, and many reflexes are "closed" here. The decrease in activity in the search and study of new objects is explained by the low level of dopamine, a mediator of pleasure that stimulates such behavior.
As for the main topic for discussion – the effect on speech, here most of the differences turned out to be insignificant, although the authors were able to find a small difference: "humanized" mice were inclined to make more individual sounds and used lower peak frequencies compared to knockout ones for one of the genes. However, this demonstrates only the role of a specific human version, and not Foxp2 as a whole.
Apparently, Foxp2 has the greatest impact on speech and sound recognition, as well as on the central regulation of speech. The most interesting thing was that mice who had not learned to speak during their lifetime told scientists after dissection: in "humanized" mice, the average length of short processes of nerve cells – dendrites – turned out to be 22% longer.
This contributes to the formation of more contacts between cells, and consequently, more efficient operation of the nervous system and, in particular, the auditory analyzer.
Thus, Enard once again confirmed the fact that evolution within such a perfect group as animals was mainly due to transcription factors, and not genes in the usual sense of the word. It remains to look for Foxp2 from parrots, and the question of its role will be finally resolved.
Portal "Eternal youth" http://vechnayamolodost.ru/01.06.2009