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招募效应蛋白的平行途径决定中心粒的驱动和抑制
作者:小柯机器人 发布时间:2021/8/28 21:12:31

美国宾夕法尼亚大学Michael A. Lampson研究团队发现,招募效应蛋白的平行途径决定中心粒的驱动和抑制。这一研究成果于2021年8月24日在线发表在国际学术期刊《细胞》上。

据研究人员介绍,自私的中心粒DNA序列在雌性减数分裂中偏向于传递给卵子。进化理论表明,中心粒蛋白的进化是为了抑制这种"中心粒驱动"的代价。在具有遗传上不同母体和父体中心粒的杂交小鼠模型中,自私的中心粒DNA利用一个动粒途径来招募作为驱动效应器的微管稳定蛋白。

研究人员表明,这种功能差异被异染色质招募效应物的平行途径所抑制,而异染色质在该系统的中心粒之间是相似的。用CENP-C的差异等位基因破坏动粒通路可以减少中心粒之间的功能差异,而用CENP-B的缺失破坏异染色质可以扩大差异。利用鼠科基因组进行的分子进化分析确定了两种途径中蛋白质的适应性进化。研究人员提出,相对于使中心粒平等化的异染色质途径,中心粒蛋白反复进化,从而尽量减少被自私DNA所利用的动粒途径,同时保持基本功能。

附:英文原文

Title: Parallel pathways for recruiting effector proteins determine centromere drive and suppression

Author: Tomohiro Kumon, Jun Ma, R. Brian Akins, Derek Stefanik, C. Erik Nordgren, Junhyong Kim, Mia T. Levine, Michael A. Lampson

Issue&Volume: 2021-08-24

Abstract: Selfish centromere DNA sequences bias their transmission to the egg in female meiosis.Evolutionary theory suggests that centromere proteins evolve to suppress costs ofthis “centromere drive.” In hybrid mouse models with genetically different maternaland paternal centromeres, selfish centromere DNA exploits a kinetochore pathway torecruit microtubule-destabilizing proteins that act as drive effectors. We show thatsuch functional differences are suppressed by a parallel pathway for effector recruitmentby heterochromatin, which is similar between centromeres in this system. Disruptingthe kinetochore pathway with a divergent allele of CENP-C reduces functional differencesbetween centromeres, whereas disrupting heterochromatin by CENP-B deletion amplifiesthe differences. Molecular evolution analyses using Murinae genomes identify adaptiveevolution in proteins in both pathways. We propose that centromere proteins have recurrentlyevolved to minimize the kinetochore pathway, which is exploited by selfish DNA, relativeto the heterochromatin pathway that equalizes centromeres, while maintaining essentialfunctions.

DOI: 10.1016/j.cell.2021.07.037

Source: https://www.cell.com/cell/fulltext/S0092-8674(21)00940-5

期刊信息
Cell:《细胞》,创刊于1974年。隶属于细胞出版社,最新IF:36.216
官方网址:https://www.cell.com/