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大脑不对称性起源理论:在固定的右移基础上叠加的表观遗传变异。

A theory of the origin of cerebral asymmetry: epigenetic variation superimposed on a fixed right-shift.

机构信息

Sane POWIC, Warneford Hospital, Oxford, UK.

出版信息

Laterality. 2010 May;15(3):289-303. doi: 10.1080/13576500902734900. Epub 2009 Mar 13.

Abstract

A theory of the genetic basis of cerebral asymmetry is outlined according to which (1) a single right-shift factor in all human individuals interacts with (2) epigenetic variation that is apparently random, transmissible between parent and child, but with a half-life extending over a small number of generations. The right-shift factor arose late (150 to 200 thousand years ago [KYA]) in hominid evolution as a mutation in the X copy of a gene pair (Protocadherin 11XY) in a region of homology between the X and Y chromosomes created by a duplication 6MYA at the chimpanzee hominid separation. The epigenetic imprint originates in the process now known as "meiotic suppression of unpaired chromosomes" (MSUC); it reflects random pairing of partly homologous X and Y chromosome regions in male meiosis, and confers species-specific diversity of cerebral structure on the human population.

摘要

根据该理论,大脑不对称的遗传基础可以概述为:(1)所有人类个体中的单一右移因子与(2)表观遗传变异相互作用,这种变异显然是随机的,可在父母与子女之间传递,但半衰期可延长至少数几代。该右移因子在人类进化中很晚(150 至 200 千年前)出现,是 X 染色体上一对基因(原钙黏蛋白 11XY)中 X 拷贝的突变,该基因位于 X 染色体和 Y 染色体之间的同源区域,由 6MYA 年在黑猩猩人类分离时的复制产生。表观遗传印记起源于现在称为“减数分裂中未配对染色体的抑制”(MSUC)的过程;它反映了雄性减数分裂中部分同源 X 和 Y 染色体区域的随机配对,并赋予人类群体特定的大脑结构多样性。

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