Signalling Laboratory, The Babraham Institute, Cambridge, UK.
Autophagy. 2020 Apr;16(4):775-776. doi: 10.1080/15548627.2020.1725405. Epub 2020 Feb 20.
For the last two decades there has been wide ranging debate about the status of macroautophagy during mitosis. Because metazoan cells undergo an "open" mitosis in which the nuclear envelope breaks down, it has been proposed that macroautophagy must be inhibited to maintain genome integrity. While many studies have agreed that the number of autophagosomes is greatly reduced in cells undergoing mitosis, there has been no consensus on whether this reflects decreased autophagosome synthesis or increased autophagosome degradation. Reviewing the literature we were concerned that many studies relied too heavily on autophagy assays that were simply not appropriate for a relatively brief event such as mitosis. Using highly dynamic omegasome markers we have recently shown unequivocally that autophagosome synthesis is repressed at the onset of mitosis and is restored once cell division is complete. This is accomplished by CDK1, the master regulator of mitosis, taking over the function of MTORC1, to ensure autophagy is repressed during mitosis.
在过去的二十年中，关于有丝分裂过程中巨自噬的状态一直存在广泛的争论。由于真核细胞经历的是核膜崩解的“开放式”有丝分裂，因此有人提出巨自噬必须被抑制以维持基因组完整性。虽然许多研究都同意在有丝分裂的细胞中，自噬体的数量大大减少，但对于这是否反映了自噬体合成的减少或自噬体降解的增加，尚未达成共识。在回顾文献时，我们担心许多研究过于依赖自噬测定，而这些测定对于相对短暂的有丝分裂事件并不合适。我们最近使用高度动态的 omegasome 标记物明确表明，自噬体的合成在有丝分裂开始时受到抑制，一旦细胞分裂完成就会恢复。这是通过 CDK1（有丝分裂的主要调节剂）接管 MTORC1 的功能来实现的，以确保有丝分裂期间抑制自噬。
