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着丝粒黏合蛋白在减数分裂 II 中的去保护作用需要 APC/C 的活性，但不需要动粒张力。

Deprotection of centromeric cohesin at meiosis II requires APC/C activity but not kinetochore tension.

机构信息

Laboratory of Chromosome Biology, Max Planck Institute of Biochemistry, Martinsried, Germany.

Biosciences Institute, Centre for Life, Times Square, Newcastle University, Newcastle upon Tyne, UK.

出版信息

EMBO J. 2021 Apr 1;40(7):e106812. doi: 10.15252/embj.2020106812. Epub 2021 Mar 1.

DOI:10.15252/embj.2020106812
PMID:33644894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8013787/
Abstract

Genome haploidization involves sequential loss of cohesin from chromosome arms and centromeres during two meiotic divisions. At centromeres, cohesin's Rec8 subunit is protected from separase cleavage at meiosis I and then deprotected to allow its cleavage at meiosis II. Protection of centromeric cohesin by shugoshin-PP2A seems evolutionarily conserved. However, deprotection has been proposed to rely on spindle forces separating the Rec8 protector from cohesin at metaphase II in mammalian oocytes and on APC/C-dependent destruction of the protector at anaphase II in yeast. Here, we have activated APC/C in the absence of sister kinetochore biorientation at meiosis II in yeast and mouse oocytes, and find that bipolar spindle forces are dispensable for sister centromere separation in both systems. Furthermore, we show that at least in yeast, protection of Rec8 by shugoshin and inhibition of separase by securin are both required for the stability of centromeric cohesin at metaphase II. Our data imply that related mechanisms preserve the integrity of dyad chromosomes during the short metaphase II of yeast and the prolonged metaphase II arrest of mammalian oocytes.

摘要

基因组单倍体化涉及在两次减数分裂过程中从染色体臂和着丝粒上依次丢失黏合蛋白。在着丝粒处，黏合蛋白的 Rec8 亚基在减数分裂 I 时免受分离酶的切割，然后被去保护以允许其在减数分裂 II 时被切割。Shugoshin-PP2A 对着丝粒黏合蛋白的保护在进化上似乎是保守的。然而，去保护被认为依赖于纺锤体力将 Rec8 保护蛋白与中期 II 处的黏合蛋白分开，以及在酵母中，依赖于 APC/C 对保护蛋白的后期 II 破坏。在这里，我们在酵母和小鼠卵母细胞的减数分裂 II 中没有姐妹动粒双取向的情况下激活了 APC/C，并发现姐妹着丝粒在这两个系统中的分离都不需要两极纺锤体力。此外，我们表明，至少在酵母中，Shugoshin 对 Rec8 的保护和 Securin 对分离酶的抑制对于中期 II 处着丝粒黏合蛋白的稳定性都是必需的。我们的数据表明，相关机制在酵母短暂的中期 II 和哺乳动物卵母细胞延长的中期 II 阻滞期间保持二联体染色体的完整性。

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