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Human gene introduced into monkey fetus leads to bigger brain

A human gene introduced into a monkey’s fetus resulted in the development of a larger, more complex brain.

Leonardo Briceno The Post Millennial
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Researchers from the Max Planck Institute of Molecular Cell Biology and Genetics in Germany and a Japanese research team from the Central Institute for Experimental Animals have taken the human gene ARHGAP11B and introduced it into a developing marmoset fetus, causing its developing neocortex to nearly double in size.

Stated differently, a human gene introduced into a monkey’s fetus resulted in the development of a larger, more complex brain.

In a release of the study, the Journal Science described its findings in its abstract:

“In the early weeks of fetal growth, the gene drove greater elaboration of neural progenitors and neocortex than is evident in the normal fetal marmoset. ARHGAP11B expression may be one cause of the more robust neocortex that characterizes the human brain.”

Back in 2015, Wieland Hunter, the founder of the Max Planck Institute, introduced the same gene into mice. At the time, the specific function of ARHGAP11B was still largely unknown and the effect that it would have on rodents wasn’t clear. What was known, however, was that the gene was in some way relate to the size of the human neocortex.

The human neocortex is vastly complex and is the largest of all vertebrate organisms, weighing in at an average of three pounds. What’s astonishing about that size however, is the amount that’s contained within those three pounds: an average of 1,274 cubic centimeters and billions of synapse and neuro connections.

Part of what makes that possible is the folding of the brain tissue, creating more surface area in a tight amount of space—a feature that many animals with less-complex brains lack. In humans, it allows for higher brain function such as speech.

When ARHGAP11B was applied to rodents, the embryo began to develop heightened numbers of neural progenitor cells, and the normally smooth cortex of mice became folded.

Hunter, who had led that study back in 2015, also played a hand in leading the application of ARHGAP11B on the marmoset fetus.

Although the project ultimately ended in the successful adoption of the gene, Hunter decided that the project would go uncontained for the time being, citing a need for more careful evaluation.

“We confined our analyses to marmoset fetuses, because we anticipated that the expression of this human-specific gene would affect the neocortex development in the marmoset,” Hunter said.

“In light of potential unforeseeable consequences with regard to postnatal brain function, we considered it a prerequisite - and mandatory from an ethical point of view - to first determine the effects of ARHGAP11B on the development of fetal marmoset neocortex.”

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