The Molecular Mechanisms of in Response to Reactive Oxygen Species Stress.

Reactive oxygen species (ROSs) are critical for the growth, development, proliferation, and pathogenicity of microbial pathogens; however, excessive levels of ROSs are toxic. Little is known about the signaling cascades in response to ROS stress in oomycetes such as , the causal agent of potato late blight. Here, was used as a model system to investigate the mechanism underlying the response to ROS stress in oomycete pathogens. Results showed severe defects in sporangium germination, mycelium growth, appressorium formation, and virulence of in response to HO stress. Importantly, these phenotypes mimic those of treated with rapamycin, the inhibitor of target of rapamycin (TOR, 1-phosphatidylinositol-3-kinase). Strong synergism occurred when was treated with a combination of HO and rapamycin, suggesting that a crosstalk exists between ROS stress and the TOR signaling pathway. Comprehensive analysis of transcriptome, proteome, and phosphorylation omics showed that HO stress significantly induced the operation of the TOR-mediated autophagy pathway. Monodansylcadaverine staining showed that in the presence of HO and rapamycin, the autophagosome level increased in a dosage-dependent manner. Furthermore, transgenic potatoes containing double-stranded RNA of in () displayed high resistance to . Therefore, TOR is involved in the ROS response and is a potential target for control of oomycete diseases, because host-mediated silencing of increases potato resistance to late blight.