Mitotic phosphorylation of the ULK complex regulates cell cycle progression
Mitotic phosphorylation of the ULK complex regulates cell cycle progression
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DOI：
10.1371/journal.pbio.3000718
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发表时间：
2020-06
期刊：
影响因子：
9.8
通讯作者：
A. Yamasaki;Yui Jin;Y. Ohsumi
中科院分区：
文献类型：
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作者：
A. Yamasaki;Yui Jin;Y. Ohsumi
自噬是一种靶向细胞器和大分子的细胞内降解途径，从而调节细胞的各种功能。磷酸化是一种重要的转录后蛋白质修饰，参与了包括自噬在内的生物学功能的调节。在异步条件下，自噬活性主要被雷帕霉素（mTOR）激酶的机制靶点抑制，但自噬相关基因（ATG）蛋白在细胞周期的整个连续阶段是否被差异磷酸化仍不清楚。在这个问题上，李和他的同事报告说，细胞周期蛋白依赖性激酶1（CDK1）磷酸化的ULK复合物在有丝分裂。这种磷酸化诱导自噬，并且令人惊讶地显示出驱动细胞周期进展。这项工作揭示了自噬在细胞周期进程中尚未被认识的作用，并增强了我们对细胞生长和增殖过程中特定的阶段依赖性自噬调控的理解。
Autophagy is an intracellular degradation pathway targeting organelles and macromolecules, thereby regulating various cellular functions. Phosphorylation is a key posttranscriptional protein modification implicated in the regulation of biological function including autophagy. Under asynchronous conditions, autophagy activity is predominantly suppressed by mechanistic target of rapamycin (mTOR) kinase, but whether autophagy-related genes (ATG) proteins are phosphorylated differentially throughout the sequential phases of the cell cycle remains unclear. In this issue, Li and colleagues report that cyclin-dependent kinase 1 (CDK1) phosphorylates the ULK complex during mitosis. This phosphorylation induces autophagy and, surprisingly, is shown to drive cell cycle progression. This work reveals a yet-unappreciated role for autophagy in cell cycle progression and enhances our understanding of the specific phase-dependent autophagy regulation during cellular growth and proliferation.