2. Academic Validation
  3. Human-specific ARHGAP11B increases size and folding of primate neocortex in the fetal marmoset

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

  • Science. 2020 Jul 31;369(6503):546-550. doi: 10.1126/science.abb2401.
Michael Heide 1,  Christiane Haffner 2,  Ayako Murayama 3 4,  Yoko Kurotaki 5,  Haruka Shinohara 5,  Hideyuki Okano 3 4,  Erika Sasaki 5,  Wieland B Huttner 1
Affiliations

Affiliations

  • 1 Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany. [email protected] [email protected].
  • 2 Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
  • 3 Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
  • 4 Laboratory for Marmoset Neural Architecture, RIKEN Center for Brain Science, Wako City, Saitama 351-0198, Japan.
  • 5 Department of Marmoset Biology and Medicine, Central Institute for Experimental Animals, Kawasaki 210-0821, Japan.
PMID: 32554627 DOI: 10.1126/science.abb2401
Abstract

The neocortex has expanded during mammalian evolution. Overexpression studies in developing mouse and ferret neocortex have implicated the human-specific gene ARHGAP11B in neocortical expansion, but the relevance for primate evolution has been unclear. Here, we provide functional evidence that ARHGAP11B causes expansion of the primate neocortex. ARHGAP11B expressed in fetal neocortex of the common marmoset under control of the gene's own (human) promoter increased the numbers of basal radial glia progenitors in the marmoset outer subventricular zone, increased the numbers of upper-layer neurons, enlarged the neocortex, and induced its folding. Thus, the human-specific ARHGAP11B drives changes in development in the nonhuman primate marmoset that reflect the changes in evolution that characterize human neocortical development.

Figures