Suppr超能文献

自噬防止失控的减数分裂。

Autophagy prevents runaway meiotic divisions.

机构信息

Department of Internal Medicine, Center for Autophagy Research, UT Southwestern Medical Center, Dallas, TX, USA.

Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, USA.

出版信息

Autophagy. 2020 May;16(5):969-970. doi: 10.1080/15548627.2020.1739449. Epub 2020 Mar 15.

Abstract

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.

摘要

在芽殖酵母中,巨自噬/自噬对于细胞进入有丝分裂至关重要。我们最近的研究表明,自噬对于有丝分裂后时期也是必需的。在细胞进入有丝分裂时抑制自噬会导致额外的纺锤体形成、纺锤体伸长和染色体异常分离,从而导致细胞死亡。在这些条件下,减数分裂 II 特异性周期蛋白 Clb3 不存在,而后期促进复合物/周期蛋白 (APC/C) 的两个底物在额外的分裂中持续存在,而不是在减数分裂 II 后被降解。我们发现翻译抑制剂 Rim4 是自噬的底物,这可以通过其在抑制 Clb3 和 APC/C 的减数分裂特异性共激活因子 Ama1 的合成中的已知作用来解释这些观察结果。综上所述,这些结果为通过有时间限制的自噬降解基因表达的主要调控因子来控制有丝分裂后时期提供了新的机制见解。

相似文献

1
Autophagy prevents runaway meiotic divisions.自噬防止失控的减数分裂。
Autophagy. 2020 May;16(5):969-970. doi: 10.1080/15548627.2020.1739449. Epub 2020 Mar 15.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验