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Upon infection, pathogens secrete effector proteins to reprogram host cells and facilitate pathogenesis. Understanding how host processes are reprogrammed during pathogen invasion is key for the development of resistant crops. In this work, we studied two Phytophthora infestans RXLR-WY effectors, PexRD31 and PexRD54, and their cooperative effect on vesicle trafficking. While PexRD54 has an established role in modulating selective autophagy, we report that PexRD31 was able to perturb vesicle trafficking leading to an increase in endosome numbers. Transient co-expression in Nicotiana benthamianashowed that these two effectors co-localized in mobile punctate bodies that accumulate at haustoria during infection. In-planta co-immunoprecipitation confirmed this association and revealed that both effectors had shared host interactors. We hypothesize that PexRD31 and PexRD54 act cooperatively to alter vesicle trafficking during infection. Current work focuses on further characterizing the association between these two effectors and how they function in concert. By dissecting the molecular mechanisms of these virulence proteins, we hope to gain a better understanding of how host processes are reprogrammed during infection and exploit this knowledge to engineer resistance in crops.
cell biology, plant-microbe interactions, pathogens, oomycetes
cell biology, plant-microbe interactions, pathogens, oomycetes
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