Human-specific ARHGAP11B increases size and folding of primate neocortex in the fetal marmoset

Author:

Heide Michael1ORCID,Haffner Christiane1ORCID,Murayama Ayako23ORCID,Kurotaki Yoko4ORCID,Shinohara Haruka4ORCID,Okano Hideyuki23ORCID,Sasaki Erika4ORCID,Huttner Wieland B.1ORCID

Affiliation:

1. Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.

2. Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.

3. Laboratory for Marmoset Neural Architecture, RIKEN Center for Brain Science, Wako City, Saitama 351-0198, Japan.

4. Department of Marmoset Biology and Medicine, Central Institute for Experimental Animals, Kawasaki 210-0821, Japan.

Abstract

Neocortex in the fetal brain Along the path of human evolution, gene duplication and divergence produced a protein, ARHGAP11B, that is found in humans but not nonhuman primates or other mammals. Heide et al. analyzed the effects of ARHGAP11B gene expression, under control of its own human-specific promoter, in the fetal marmoset (see the Perspective by Dehay and Kennedy). 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. Science , this issue p. 546 ; see also p. 506

Funder

European Research Council

Deutsche Forschungsgemeinschaft

ERA-NET Neuron

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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