MOE Key Laboratory & Guangdong Provincial Key Laboratory of Laser Life Science, Guangzhou Key Laboratory of Spectral Analysis and Functional Probes, College of Biophotonics, Guangdong Provincial Key Laboratory of Biotechnology for Plant Development, School of Life Sciences, South China Normal University, Guangzhou, China.
School of Life Sciences, Centre for Cell & Developmental Biology and State Key Laboratory of Agrobiotechnology, Chinese University of Hong Kong, Hong Kong, China.
Nat Plants. 2023 May;9(5):749-765. doi: 10.1038/s41477-023-01398-w. Epub 2023 Apr 20.
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.
高于最佳生长温度的环境通常被称为热应激(HS),会对生物体的生存造成挑战,因为它会干扰基本的生理功能并破坏细胞组织。先前的研究已经阐明了植物 HS 响应中涉及的复杂转录调控网络,但植物适应 HS 过程中细胞器重塑和动态平衡的机制仍不清楚。在这里,我们报告了 ATG8 在调节植物高尔基体在 HS 损伤后的修复中的非典型功能。短期急性 HS 会导致高尔基体空泡化和 ATG8 向扩张的高尔基体膜易位。ATG 共轭系统的失活,而不是自噬起始物的上游失活,会消除 ATG8 对肿胀高尔基体的靶向,导致 HS 后高尔基体恢复延迟。使用基于 TurboID 的邻近标记,我们通过 AIM-LDS 界面鉴定了 CLATHRIN LIGHT CHAIN 2(CLC2)作为 ATG8 的相互作用伙伴。ATG8 将 CLC2 募集到潴泡膜上,以促进高尔基体的重新组装。总的来说,我们的研究揭示了植物细胞中高尔基体从 HS 中恢复的一个迄今为止尚未预料到的过程,并揭示了一种涉及 ATG8 的以前未知的细胞器弹性机制。