Autophagy is a central part of immunity and hence is a key target of pathogens. However, the precise molecular mechanisms by which plant pathogens manipulate autophagy remain elusive. We identify a network of 88 interactions between 184 effectors from bacterial, fungal, oomycete, and nematode pathogens with 25 Arabidopsis autophagy (ATG) proteins. Notably, Pseudomonas syringae pv tomato (Pto) bacterial effectors HrpZ1, HopF3, and AvrPtoB employ distinct molecular strategies to modulate autophagy. Calcium-dependent HrpZ1 oligomerization targets ATG4b-mediated cleavage of ATG8 to enhance autophagy, while HopF3 also targets ATG8 but suppresses autophagy, with both effectors promoting infection. AvrPtoB affects ATG1 kinase phosphorylation and enhances bacterial virulence. Since pathogens inject limited numbers of effectors into hosts, our findings establish autophagy as a key target during infection. Additionally, as autophagy is enhanced and inhibited by these effectors, autophagy likely has different functions throughout infection and, thus, must be temporally and precisely regulated for successful infection.

自噬是免疫力的重要组成部分，因此是病原体的关键靶标。但是，植物病原体操纵自噬的确切分子机制仍然难以捉摸。我们确定了细菌，真菌，卵菌和线虫病原体与25种拟南芥自噬（ATG）蛋白中的184个效应子之间的88个相互作用的网络。值得注意的是，丁香假单胞菌光伏番茄（Pto细菌效应子HrpZ1，HopF3和AvrPtoB采用不同的分子策略来调节自噬。钙依赖性HrpZ1寡聚以ATG4b介导的ATG8裂解为目标，以增强自噬，而HopF3也以ATG8为目标，但抑制自噬，这两个效应子均促进感染。AvrPtoB影响ATG1激酶的磷酸化并增强细菌毒力。由于病原体将有限数量的效应子注入宿主，因此我们的发现将自噬作为感染期间的关键靶标。另外，由于自噬被这些效应子增强和抑制，自噬在整个感染过程中可能具有不同的功能，因此必须在时间和精确度上进行调节才能成功感染。