We explored the potential for autophagy to regulate budding yeast meiosis. Following pre-meiotic DNA replication, we blocked autophagy by chemical inhibition of Atg1 kinase or engineered degradation of Atg14 and observed homologous chromosome segregation followed by sister chromatid separation; cells then underwent additional rounds of spindle formation and disassembly without DNA re-replication, leading to aberrant chromosome segregation. Analysis of cell-cycle regulators revealed that autophagy inhibition prevents meiosis II-specific expression of Clb3 and leads to the aberrant persistence of Clb1 and Cdc5, two substrates of a meiotic ubiquitin ligase activated by Ama1. Lastly, we found that during meiosis II, autophagy degrades Rim4, an amyloid-like translational repressor whose timed clearance regulates protein production from its mRNA targets, which include CLB3 and AMA1. Strikingly, engineered Clb3 or Ama1 production restored meiotic termination in the absence of autophagy. Thus, autophagy destroys a master regulator of meiotic gene expression to enable irreversible meiotic exit.

中文翻译：

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淀粉样样翻译阻遏物的自噬调节减数分裂出口。

我们探索了自噬调节发芽酵母减数分裂的潜力。减数分裂前的DNA复制后，我们通过化学抑制Atg1激酶或Atg14的工程降解来阻止自噬，并观察到同源染色体分离，然后进行姐妹染色单体分离。然后，细胞再经过几轮纺锤体形成和分解，而没有DNA复制，从而导致异常的染色体分离。细胞周期调节因子的分析表明，自噬抑制作用可阻止减数分裂II特异性表达Clb3，并导致Clb1和Cdc5异常持久化，这是Ama1激活的减数分裂泛素连接酶的两个底物。最后，我们发现在减数分裂II期间，自噬会降解Rim4，Rim4是一种淀粉样样的翻译阻遏物，其定时清除可调节其mRNA靶标产生的蛋白质，其中包括CLB3和AMA1。引人注目的是，在没有自噬的情况下，工程改造的Clb3或Ama1产物恢复了减数分裂终止。因此，自噬破坏了减数分裂基因表达的主调节器，以使不可逆的减数分裂退出。