The Potato MAP3K StVIK Is Required for the Phytophthora infestans RXLR Effector Pi17316 to Promote Disease

Plant pathogens deliver effectors to manipulate processes in their hosts, creating an environment for disease. Yet little is known about the host proteins that are targeted by effectors from filamentous pathogens. We show that both stable transgenic expression in potato and transient expression in Nicotiana benthamiana of the RXLR effector Pi17316 enhance leaf colonization by the late blight pathogen Phytophthora infestans. Expression of Pi17316 also attenuates cell death triggered by the pathogen-associated molecular pattern INF1, indicating that the effector suppresses pattern-triggered immunity. However, this effector does not attenuate cell death triggered by CF4/AVR4, Rx/PVX-CP or R3a/AVR3a, showing that it specifically suppresses INF1-triggered cell death (ICD). Pi17316 interacts directly in yeast two-hybrid assays with the potato (Solanum tuberosum) orthologue of BRL2/VH1-interacting kinase (StVIK), encoding a predicted mitogen-activated protein kinase kinase kinase (MAP3K). Interaction in planta was confirmed by co-immunoprecipitation and demonstrated to occur at the plant plasma membrane. Virus-induced gene silencing (VIGS) of VIK in N. benthamiana attenuated P. infestans colonization, whereas transient overexpression of StVIK enhanced P. infestans colonization, indicating that this host protein acts as a susceptibility (S) factor. Moreover, VIK overexpression specifically attenuated ICD, indicating it is a negative regulator of immunity. The abilities of Pi17316 to enhance P. infestans colonization or suppress ICD were significantly compromised in NbVIK-silenced plants, demonstrating that Pi17316 effector activity is mediated by this MAP3K. Thus, StVIK is exploited by P. infestans as an S factor to promote late blight disease.