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Autophagy prevents runaway meiotic divisions.
Autophagy ( IF 14.6 ) Pub Date : 2020-03-09 , DOI: 10.1080/15548627.2020.1739449
Fei Wang 1 , Vladimir Denic 2 , Soni Lacefield 3
Affiliation  

In budding yeast, macroautophagy/autophagy is required for cells to enter into the meiotic divisions. Our recent publication showed that autophagy is also required for meiotic exit. Inhibition of autophagy as cells enter into the meiotic divisions results in additional rounds of spindle formation, spindle elongation, and aberrant chromosome segregation leading to cell death. Under these conditions, the meiosis II-specific cyclin Clb3 is absent, and two substrates of the anaphase-promoting complex/cyclosome (APC/C) persist into the additional divisions instead of being degraded after meiosis II. We found that the translational repressor Rim4 is a substrate of autophagy, which could explain these observations through its known role in repressing synthesis of Clb3 and the meiosis-specific co-activator of the APC/C, Ama1. Combined, these results provide new mechanistic insight into the control of meiotic exit through timed autophagic degradation of a master regulator of gene expression.



中文翻译:


自噬可防止减数分裂失控。



在芽殖酵母中,细胞进入减数分裂需要巨自噬/自噬。我们最近发表的文章表明,自噬也是减数分裂退出所必需的。当细胞进入减数分裂时,自噬的抑制会导致额外轮次的纺锤体形成、纺锤体伸长和异常染色体分离,从而导致细胞死亡。在这些条件下,减数分裂 II 特异性细胞周期蛋白 Clb3 不存在,并且后期促进复合物/环体 (APC/C) 的两种底物持续进入额外的分裂,而不是在减数分裂 II 后被降解。我们发现翻译抑制子 Rim4 是自噬的底物,这可以通过其在抑制 Clb3 和 APC/C 减数分裂特异性共激活子 Ama1 合成中的已知作用来解释这些观察结果。综合起来,这些结果为通过基因表达主调节因子的定时自噬降解来控制减数分裂退出提供了新的机制见解。

更新日期:2020-03-10
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