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.

自噬是一种针对细胞器和大分子的细胞内降解途径，从而调节多种细胞功能。磷酸化是一种关键的转录后蛋白质修饰，涉及包括自噬在内的生物功能的调节。在异步条件下，自噬活性主要受到雷帕霉素靶标 (mTOR) 激酶的抑制，但自噬相关基因 (ATG) 蛋白是否在细胞周期的连续阶段中被差异磷酸化仍不清楚。在本期中，Li 及其同事报告说，细胞周期蛋白依赖性激酶 1 (CDK1) 在有丝分裂过程中磷酸化 ULK 复合物。这种磷酸化会诱导自噬，并且令人惊讶的是，它被证明可以驱动细胞周期进程。这项工作揭示了自噬在细胞周期进程中尚未被认识到的作用，并增强了我们对细胞生长和增殖过程中特定阶段依赖性自噬调节的理解。