Hydrogen sulfide (H₂S) is an endogenously generated gaseous signaling molecule, which recently has been implicated in autophagy regulation in both plants and mammals through persulfidation of specific targets. Persulfidation has been suggested as the molecular mechanism through which sulfide regulates autophagy in plant cells. ATG18a is a core autophagy component that is required for bulk autophagy and also for reticulophagy during endoplasmic reticulum (ER) stress. In this research, we revealed the role of sulfide in plant ER stress responses as a negative regulator of autophagy. We demonstrate that sulfide regulates ATG18a phospholipid-binding activity by reversible persulfidation at Cys103, and that this modification activates ATG18a binding capacity to specific phospholipids in a reversible manner. Our findings strongly suggest that persulfidation of ATG18a at C103 regulates autophagy under ER stress, and that the impairment of persulfidation affects both the number and size of autophagosomes.

硫化氢（H ₂S) 是一种内源性气体信号分子，最近它通过特定靶标的过硫化作用参与植物和哺乳动物的自噬调节。过硫化被认为是硫化物调节植物细胞自噬的分子机制。ATG18a 是一种核心自噬成分，是大量自噬和内质网 (ER) 应激期间的网状自噬所必需的。在这项研究中，我们揭示了硫化物在植物内质网应激反应中作为自噬负调节剂的作用。我们证明硫化物通过 Cys103 处的可逆过硫化作用调节 ATG18a 磷脂结合活性，并且这种修饰以可逆方式激活 ATG18a 与特定磷脂的结合能力。