To be successful plant pathogens, microbes use ‘effector proteins’ to manipulate host functions to their benefit. Identifying host targets of effector proteins, and characterising their role in the infection process, allows us to better understand plant-pathogen interactions and the plant immune system. Yeast-2-hybrid and co-immunoprecipitation were used to demonstrate that Phytophthora infestans effector PiAVR2 interacts with all three BSU1-like (BSL) family members from Solanum tuberosum. Transient expression of BSL1, 2 and 3 enhanced P. infestans leaf infection. BSL1 and BSL3 suppressed INF1 elicitin-triggered cell death, showing that they negatively regulate immunity. Virus-induced gene silencing studies revealed that BSL2 and 3 are required for BSL1 stability, and show that basal levels of immunity are increased in BSL-silenced plants. Immune suppression by BSL family members is dependent on the brassinosteroid-responsive host transcription factor CHL1. P. infestans effector PiAVR2 targets all three BSL family members in the crop plant S. tuberosum. These phosphatases, known for their role in growth-promoting brassinosteroid signalling, all support P. infestans virulence, and thus can be regarded as susceptibility factors in late blight infection.
- Plant immunity
- effector-triggered susceptibility
- plant disease
- Late blight
- Plant pathogens