Spindle assembly checkpoint of oocytes depends on a kinetochore structure determined by cohesin in meiosis I.
Spindle assembly checkpoint of oocytes depends on a kinetochore structure determined by cohesin in meiosis I.
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DOI：
10.1016/j.cub.2013.10.052
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发表时间：
2013-12-16
期刊：
影响因子：
9.2
通讯作者：
Nasmyth, Kim
中科院分区：
文献类型：
--
作者：
Tachibana-Konwalski, Kikue;Godwin, Jonathan;Borsos, Mate;Rattani, Ahmed;Adams, David J.;Nasmyth, Kim
由于分离酶和细胞周期蛋白 B 破坏对姐妹染色单体内聚力的溶解是不可逆的，因此必须延迟两者，直到所有染色体在有丝分裂纺锤体上双向取向。未正确附着在纺锤体上的动粒会产生有丝分裂检查点复合体 (MCC)，它会抑制后期促进复合体/环体 (APC/C) 并阻止后期开始。此过程称为主轴装配检查点 (SAC)。 SAC 在减数分裂 I 中尤其重要，其中二价体由同源染色体组成，通过 chiasmata bioorient 连接在一起。由于第一次减数分裂不受罕见的不对称染色体或错位二价染色体的影响，因此认为需要几个无张力动粒来产生足够的 MCC 来抑制 APC/C。与此一致的是，缺乏交叉的单价体在 Mlh1−/− 卵母细胞中引起 SAC 介导的停滞。相比之下，Rec8TEV/TEV 卵母细胞中 TEV 蛋白酶诱导的粘连蛋白裂解产生的染色单体仅延迟 APC/C 激活。由于 TEV 蛋白酶减轻了 Mlh1−/−Rec8TEV/TEV 卵母细胞的停滞，即使靶向着丝粒，我们得出结论，它们的 SAC 依赖于粘连蛋白以及专用着丝粒蛋白。这对老化卵母细胞具有重要意义，其中粘连蛋白退化将诱导姐妹动粒生物取向并损害 MCC 的产生，导致染色体错误分离和非整倍体胎儿。粘连蛋白对于减数分裂中强大的纺锤体组装检查点活性是必需的 粘连蛋白对纺锤体组装检查点的依赖性是减数分裂特异性的 着丝粒粘连对于姐妹动粒单向是必要的
Since the dissolution of sister chromatid cohesion by separase and cyclin B destruction is irreversible, it is essential to delay both until all chromosomes have bioriented on the mitotic spindle. Kinetochores that are not correctly attached to the spindle generate the mitotic checkpoint complex (MCC), which inhibits the anaphase-promoting complex/cyclosome (APC/C) and blocks anaphase onset. This process is known as the spindle assembly checkpoint (SAC). The SAC is especially important in meiosis I, where bivalents consisting of homologous chromosomes held together by chiasmata biorient. Since the first meiotic division is unaffected by rare achiasmatic chromosomes or misaligned bivalents, it is thought that several tensionless kinetochores are required to produce sufficient MCC for APC/C inhibition. Consistent with this, univalents lacking chiasmata elicit a SAC-mediated arrest in Mlh1−/− oocytes. In contrast, chromatids generated by TEV protease-induced cohesin cleavage in Rec8TEV/TEV oocytes merely delay APC/C activation. Since the arrest of Mlh1−/−Rec8TEV/TEV oocytes is alleviated by TEV protease, even when targeted to kinetochores, we conclude that their SAC depends on cohesin as well as dedicated kinetochore proteins. This has important implications for aging oocytes, where cohesin deterioration will induce sister kinetochore biorientation and compromise MCC production, leading to chromosome missegregation and aneuploid fetuses. Cohesin is necessary for robust spindle assembly checkpoint activity in meiosis I Cohesin dependence of the spindle assembly checkpoint is meiosis specific Centromeric cohesion is necessary for sister kinetochore mono-orientation
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DOI：
10.1083/jcb.43.1.40
发表时间：
1969-10
期刊：
The Journal of cell biology
影响因子：
--
作者：
Nicklas RB;Koch CA
通讯作者：
Koch CA
影响因子：
21.3
作者：
Nilsson, Jakob;Yekezare, Mona;Minshull, Jeremy;Pines, Jonathon
通讯作者：
Pines, Jonathon
影响因子：
3.8
作者：
Homer, HA;McDougall, A;Herbert, M
通讯作者：
Herbert, M
影响因子：
4.6
作者：
Lane, Simon I. R.;Yun, Yan;Jones, Keith T.
通讯作者：
Jones, Keith T.
影响因子：
9.2
作者：
Nagaoka, So Iha;Hodges, Craig A.;Albertini, David F.;Hunt, Patricia Ann
通讯作者：
Hunt, Patricia Ann