Autophagy is critical for plant defense against necrotrophic pathogens, which causes serious yield loss on crops. However, the post-translational regulatory mechanisms of autophagy pathway in plant resistance against necrotrophs remain poorly understood. In this study, we report that phosphorylation modification on ATG18a, a key regulator of autophagosome formation in Arabidopsis thaliana, constitutes a post-translation regulation of autophagy, which attenuates plant resistance against necrotrophic pathogens. We found that phosphorylation of ATG18a suppresses autophagosome formation and its subsequent delivery into the vacuole, which results in reduced autophagy activity and compromised plant resistance against Botrytis cinerea. In contrast, overexpression of ATG18a dephosphorylation-mimic form increases the accumulation of autophagosomes and complements the plant resistance of atg18a mutant against B. cinerea. Moreover, BAK1, a key regulator in plant resistance, was identified to physically interact with and phosphorylate ATG18a. Mutation of BAK1 blocks ATG18a phosphorylation at four of the five detected phosphorylation sites after B. cinerea infection and strongly activates autophagy, leading to enhanced resistance against B. cinerea. Collectively, the identification of functional phosphorylation sites on ATG18a and the corresponding kinase BAK1 unveiled how plant regulates autophagy during resistance against necrotrophic pathogens.

自噬对于植物防御坏死性病原体至关重要，这会导致农作物严重减产。然而，自噬通路的翻译后调控机制在植物对坏死菌的抗性中仍然知之甚少。在这项研究中，我们报告说，对拟南芥自噬体形成的关键调节剂ATG18a的磷酸化修饰，构成了自噬的翻译后调控，减弱了植物对坏死性病原体的抗性。我们发现，ATG18a的磷酸化抑制了自噬体的形成及其随后的传递进入液泡，从而导致自噬活性降低并损害了对灰葡萄孢的植物抗性。。与此相反，ATG18a去磷酸化模拟物形式的过表达增加了自噬体的积累和补充的植物抗性atg18a突变体对抗灰葡萄孢。此外，已确定BAK1是植物抗性的关键调控因子，可与ATG18a发生物理相互作用并使其磷酸化。BAK1突变会在灰葡萄孢菌感染后在五个检测到的磷酸化位点中的四个位点阻滞ATG18a磷酸化，并强烈激活自噬，导致增强的对灰葡萄孢菌的抗性。总的来说，对ATG18a和相应的激酶BAK1上的功能性磷酸化位点的鉴定揭示了植物如何在抵抗坏死性病原体的过程中调节自噬。