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着丝粒驱动的细胞机制和后果。

The cellular mechanisms and consequences of centromere drive.

机构信息

Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, USA; Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, USA.

Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, USA; Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, USA. Electronic address: mailto:

出版信息

Curr Opin Cell Biol. 2018 Jun;52:58-65. doi: 10.1016/j.ceb.2018.01.011. Epub 2018 Feb 16.

Abstract

During female meiosis, only one of four meiotic products is retained in the egg. It was previously proposed that chromosomes might compete for inclusion in the egg via their centromere 'strength'. Recent findings have revealed the primary requirements for such 'centromere drive'. First, CDC42 signaling from the oocyte cortex renders the meiotic I spindle asymmetric. Second, 'stronger' centromeres preferentially detach from microtubules in cortical proximity, making them more likely to orient away from the cortex, and be included in the egg. Third, centromeric satellite DNA expansions result in greater recruitment of centromeric proteins. Despite these mechanistic insights, it is still unclear if centromere drive elicits rapid evolution of centromeric proteins, thereby driving cellular incompatibilities and wreaking havoc on centromere stability.

摘要

在雌性减数分裂过程中,四个减数分裂产物中只有一个被保留在卵子中。此前有人提出,染色体可能通过其着丝粒“强度”来竞争被包含在卵子中。最近的研究结果揭示了这种“着丝粒驱动”的主要要求。首先,卵母细胞皮层中的 CDC42 信号使减数分裂 I 纺锤体不对称。其次,“更强”的着丝粒优先从皮质附近的微管上脱离,这使它们更有可能远离皮层,并被包含在卵子中。第三,着丝粒卫星 DNA 的扩展导致更多的着丝粒蛋白被招募。尽管有这些机制上的见解,但仍不清楚着丝粒驱动是否会引发着丝粒蛋白的快速进化,从而导致细胞不兼容,并破坏着丝粒稳定性。

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