Autophagy and cap-dependent mRNA translation are tightly regulated by the mechanistic target of rapamycin complex 1 (mTORC1) signalling complex in response to nutrient availability. However, the regulation of these processes, and mTORC1 itself, is different during mitosis, and this has remained an area of significant controversy; for example, studies have argued that autophagy is either repressed or highly active during mitosis. Recent studies have shown that autophagy initiation is repressed, and cap-dependent mRNA translation is maintained during mitosis despite mTORC1 activity being repressed. This is achieved in large part by a switch from mTORC1- to cyclin-dependent kinase 1 (CDK1)–mediated regulation. Here, we review the history and recent advances and seek to present a unifying model to inform the future study of autophagy and mTORC1 during mitosis.

自噬和帽依赖性 mRNA 翻译受到雷帕霉素复合物 1 (mTORC1) 信号复合物的机制靶点的严格调控，以响应营养可用性。然而，这些过程的调节以及 mTORC1 本身在有丝分裂期间是不同的，这仍然是一个存在重大争议的领域。例如，研究认为自噬在有丝分裂过程中要么受到抑制，要么高度活跃。最近的研究表明，自噬起始受到抑制，尽管 mTORC1 活性受到抑制，但在有丝分裂期间仍保持帽依赖性 mRNA 翻译。这在很大程度上是通过从 mTORC1 到细胞周期蛋白依赖性激酶 1 (CDK1) 介导的调节的转换来实现的。这里，