Neocortical neurogenesis in development and evolution—Human-specific features,The Journal of Comparative Neurology

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Neocortical neurogenesis in development and evolution—Human-specific features
The Journal of Comparative Neurology ( IF 2.3 ) Pub Date : 2024-01-08 , DOI: 10.1002/cne.25576
Wieland B Huttner ₁ , Michael Heide ₂ , Felipe Mora-Bermúdez ₁ , Takashi Namba ₃

Affiliation

In this review, we focus on human-specific features of neocortical neurogenesis in development and evolution. Two distinct topics will be addressed. In the first section, we discuss the expansion of the neocortex during human evolution and concentrate on the human-specific gene ARHGAP11B. We review the ability of ARHGAP11B to amplify basal progenitors and to expand a primate neocortex. We discuss the contribution of ARHGAP11B to neocortex expansion during human evolution and its potential implications for neurodevelopmental disorders and brain tumors. We then review the action of ARHGAP11B in mitochondria as a regulator of basal progenitor metabolism, and how it promotes glutaminolysis and basal progenitor proliferation. Finally, we discuss the increase in cognitive performance due to the ARHGAP11B-induced neocortical expansion. In the second section, we focus on neocortical development in modern humans versus Neanderthals. Specifically, we discuss two recent findings pointing to differences in neocortical neurogenesis between these two hominins that are due to a small number of amino acid substitutions in certain key proteins. One set of such proteins are the kinetochore-associated proteins KIF18a and KNL1, where three modern human-specific amino acid substitutions underlie the prolongation of metaphase during apical progenitor mitosis. This prolongation in turn is associated with an increased fidelity of chromosome segregation to the apical progenitor progeny during modern human neocortical development, with implications for the proper formation of radial units. Another such key protein is transketolase-like 1 (TKTL1), where a single modern human-specific amino acid substitution endows TKTL1 with the ability to amplify basal radial glia, resulting in an increase in upper-layer neuron generation. TKTL1's ability is based on its action in the pentose phosphate pathway, resulting in increased fatty acid synthesis. The data imply greater neurogenesis during neocortical development in modern humans than Neanderthals due to TKTL1, in particular in the developing frontal lobe.

中文翻译：

发育和进化中的新皮质神经发生——人类特有的特征

在这篇综述中，我们重点关注新皮质神经发生在发育和进化中的人类特异性特征。将讨论两个不同的主题。在第一部分中，我们讨论人类进化过程中新皮质的扩展，并重点关注人类特有的基因ARHGAP11B 。我们回顾了 ARHGAP11B 扩增基底祖细胞和扩展灵长类新皮质的能力。我们讨论了ARHGAP11B在人类进化过程中对新皮质扩张的贡献及其对神经发育障碍和脑肿瘤的潜在影响。然后我们回顾了 ARHGAP11B 在线粒体中作为基础祖细胞代谢调节剂的作用，以及它如何促进谷氨酰胺分解和基础祖细胞增殖。最后，我们讨论了 ARHGAP11B 诱导的新皮质扩张导致的认知能力的提高。在第二部分中，我们重点关注现代人类与尼安德特人的新皮质发育。具体来说，我们讨论了最近的两项发现，指出这两种古人类之间新皮质神经发生的差异是由于某些关键蛋白质中的少量氨基酸取代造成的。一组此类蛋白质是动粒相关蛋白 KIF18a 和 KNL1，其中三个现代人类特异性氨基酸取代是顶端祖细胞有丝分裂中期延长的基础。这种延长反过来又与现代人类新皮质发育过程中顶端祖细胞后代染色体分离的保真度增加有关，这对径向单位的正确形成具有影响。另一个这样的关键蛋白是转酮醇酶样 1 (TKTL1)，其中单个现代人类特异性氨基酸取代赋予 TKTL1 扩增基底放射状胶质细胞的能力，从而导致上层神经元生成的增加。 TKTL1 的能力基于其在磷酸戊糖途径中的作用，导致脂肪酸合成增加。这些数据表明，由于 TKTL1，现代人类新皮质发育过程中的神经发生比尼安德特人更大，特别是在发育中的额叶。

更新日期：2024-01-08

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