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 Tests in marmosets solidify the link between a human-specific gene and the thicker brain neocortex characteristic of humans. 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.

中文翻译：

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人类特异性 ARHGAP11B 增加胎狨猴灵长类新皮质的大小和折叠

胎儿大脑中的新皮质在人类进化的道路上，基因复制和分化产生了一种蛋白质 ARHGAP11B，它在人类中发现，但在非人类灵长类动物或其他哺乳动物中没有。海德等人。分析了 ARHGAP11B 基因表达的影响，在其自身的人类特异性启动子的控制下，在胎狨猴中（见 Dehay 和 Kennedy 的观点）。在胎儿生长的最初几周，与正常胎儿狨猴相比，该基因驱动神经祖细胞和新皮质的精细加工。ARHGAP11B 表达可能是人类大脑特征性更强的新皮质的原因之一。科学，这个问题 p。546; 另见第 506 在狨猴中的测试巩固了人类特定基因与人类较厚的大脑新皮质特征之间的联系。在哺乳动物进化过程中，新皮层已经扩张。小鼠和雪貂新皮质发育中的过度表达研究表明人类特异性基因 ARHGAP11B 与新皮质扩张有关，但与灵长类动物进化的相关性尚不清楚。在这里，我们提供了 ARHGAP11B 导致灵长类新皮层扩张的功能证据。ARHGAP11B 在基因自身（人类）启动子控制下的普通狨猴胎儿新皮层中表达，增加了狨猴外脑室下区基底径向胶质祖细胞的数量，增加了上层神经元的数量，扩大了新皮质，并诱导了其折叠式的。因此，人类特有的 ARHGAP11B 驱动了非人类灵长类狨猴的发育变化，这反映了人类新皮质发育特征的进化变化。