Abstract
To be successful plant pathogens, microbes use "effector proteins" to manipulate host functions to their benefit. Identifying host targets of effector proteins and characterizing their role in the infection process allow us to better understand plant-pathogen interactions and the plant immune system. Yeast two-hybrid analysis and coimmunoprecipitation were used to demonstrate that the Phytophthora infestans effector AVIRULENCE 2 (PiAVR2) interacts with all three BRI1-SUPPRESSOR1-like (BSL) family members from potato (Solanum tuberosum). Transient expression of BSL1, BSL2, and BSL3 enhanced P. infestans leaf infection. BSL1 and BSL3 suppressed INFESTIN 1 elicitin-triggered cell death, showing that they negatively regulate immunity. Virus-induced gene silencing studies revealed that BSL2 and BSL3 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 CIB1/HBI1-like 1. The 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 signaling, all support P. infestans virulence and thus can be regarded as susceptibility factors in late blight infection.
Highlights
In this work we have determined that the P. infestans effector PiAVR2 targets all three members of the BSL family in S. tuberosum: StBSL1, StBSL2, and StBSL3 (Figure 1)
P. infestans, identifying these proteins as susceptibility (S) factors in late blight infection (Figure 5b). This family of kelch-repeat phosphatases is homologous to Arabidopsis BSU1, characterized as a positive regulator in the growth-promoting brassinosteroid signaling pathway
Previous work had established that PiAVR2 interacts with StBSL1 (Saunders et al, 2012) and that PiAVR2 upregulates brassinosteroid-induced genes, exploiting the crosstalk that exists between growth and immunity in plants (Turnbull and Yang et al, 2017)
Summary
Plants are constantly challenged by microbes, such as bacteria, fungi, and oomycetes, the majority of which are nonpathogenic by virtue of the highly effective plant immune system. All three phosphatases are capable of enhancing P. infestans virulence when overexpressed, identifying the StBSL proteins as susceptibility factors in late blight infection This is not a straightforward case of redundancy; there are functional differences and regulatory interactions between BSL family members at both the gene expression and the protein levels. StBSL1 has been shown to be required for PiAVR2 recognition by the NB-LRR protein R2, with BSL1 silencing in N. benthamiana resulting in a significant decrease in R2-mediated hypersensitive response (HR) (Saunders et al, 2012). A pronounced increase in ICD was observed in NbBSL2/3-silenced plants (Figure 3) This suggests that negative regulation of PTI has been removed or reduced, allowing a stronger response to PAMP recognition. While StBSL1 was still able to achieve moderate, albeit significantly reduced, suppression in the CHL1-silenced plants, StBSL3 was unable to suppress ICD at all (Figure 7)
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