bims-nocaut Biomed News
on Non-canonical autophagy
Issue of 2023–04–23
two papers selected by
Quentin Frenger, University of Strasbourg
  1. Phagophore-lysosome/vacuole fusion in mutant yeast and mammalian cells.
  2. A non-canonical role of ATG8 in Golgi recovery from heat stress in plants.
  1. Autophagy. 2023 Apr 21.
    Phagophore-lysosome/vacuole fusion in mutant yeast and mammalian cells.
    Yongheng Liang.
      Macroautophagy/autophagy is a process through which the phagophores engulf non-essential or damaged cellular materials, forming double-membrane autophagosomes (APs) and fusing with lysosomes/vacuoles, after which the materials are degraded for recycling purposes. Autophagy is associated with increased cell survival under different stress conditions. AP-lysosome/vacuole fusion is a critical step in autophagy. Some mutant cells can accumulate phagophores under autophagy-induction conditions. Autophagy is interrupted when accumulated phagophores cannot fuse with lysosomes/vacuoles, resulting in a significant decrease in cell survivability. However, phagophore-lysosome/vacuole fusion has been reported in related mammalian cells and yeast mutant cells. This observation indicates that it is possible to restore a partial autophagy process after interruption. Furthermore, these findings indicate that phagophore closure is not a prerequisite for its fusion with the lysosome/vacuole in the mutant cells. The phagophore-lysosome/vacuole fusion strategy can significantly rescue defective autophagy due to failed phagophore closure. This commentary discusses the fusion of phagophores and lysosomes/vacuoles and implications of such fusion events.
    Keywords:  autolysosome; autophagic body; autophagosome; inner membrane of phagophore or autophagosome; lysosome; outer membrane of phagophore or autophagosome; phagophore; phagophore-lysosome/vacuole fusion; sporulation; vacuole
    DOI:  https://doi.org/10.1080/15548627.2023.2205272
  2. Nat Plants. 2023 Apr 20.
    A non-canonical role of ATG8 in Golgi recovery from heat stress in plants.
    Jun Zhou, Juncai Ma, Chao Yang, Xiu Zhu, Jing Li, Xuanang Zheng, Xibao Li, Siyu Chen, Lei Feng, Pengfei Wang, Man Ip Ho, Wenlong Ma, Jun Liao, Faqiang Li, Chao Wang, Xiaohong Zhuang, Liwen Jiang, Byung-Ho Kang, Caiji Gao.
      Above-optimal growth temperatures, usually referred to as heat stress (HS), pose a challenge to organisms' survival as they interfere with essential physiological functions and disrupt cellular organization. Previous studies have elucidated the complex transcriptional regulatory networks involved in plant HS responses, but the mechanisms of organellar remodelling and homeostasis during plant HS adaptations remain elusive. Here we report a non-canonical function of ATG8 in regulating the restoration of plant Golgi damaged by HS. Short-term acute HS causes vacuolation of the Golgi apparatus and translocation of ATG8 to the dilated Golgi membrane. The inactivation of the ATG conjugation system, but not of the upstream autophagic initiators, abolishes the targeting of ATG8 to the swollen Golgi, causing a delay in Golgi recovery after HS. Using TurboID-based proximity labelling, we identified CLATHRIN LIGHT CHAIN 2 (CLC2) as an interacting partner of ATG8 via the AIM-LDS interface. CLC2 is recruited to the cisternal membrane by ATG8 to facilitate Golgi reassembly. Collectively, our study reveals a hitherto unanticipated process of Golgi stack recovery from HS in plant cells and uncovers a previously unknown mechanism of organelle resilience involving ATG8.
    DOI:  https://doi.org/10.1038/s41477-023-01398-w
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