TY - JOUR T1 - Human-specific <em>ARHGAP11B</em> is necessary and sufficient for human-type basal progenitor levels in primate brain organoids JF - bioRxiv DO - 10.1101/2020.10.01.322792 SP - 2020.10.01.322792 AU - Jan Fischer AU - Jula Peters AU - Takashi Namba AU - Wieland B. Huttner AU - Michael Heide Y1 - 2020/01/01 UR - http://biorxiv.org/content/early/2020/10/01/2020.10.01.322792.abstract N2 - Based on studies in various animal models, including developing ferret neocortex (Kalebic et al., 2018), the human-specific gene ARHGAP11B has been implicated in human neocortex expansion. However, the extent of its contribution to this expansion during primate evolution is unknown. Here we addressed this issue by genetic manipulation of ARHGAP11B levels and function in chimpanzee and human cerebral organoids. Interference with ARHGAP11B’s function in human cerebral organoids caused a massive decrease, down to a chimpanzee level, in the proliferation and abundance of basal progenitors, the progenitors thought to have a key role in neocortex expansion. Conversely, ARHGAP11B expression in chimpanzee cerebral organoids resulted in a doubling of cycling basal progenitors. Taken together, our findings demonstrate that ARHGAP11B is necessary and sufficient to maintain the elevated basal progenitor levels that characterize the fetal human neocortex, suggesting that this human-specific gene was a major contributor to neocortex expansion during human evolution. ER -