A bacterial effector counteracts host autophagy by promoting degradation of an autophagy component
Jia Xuan Leong, Margot Raffeiner, Daniela Spinti, Gautier Langin, Mirita Franz‐Wachtel, Andrew R. Guzman, Jung‐Gun Kim, Pooja Pandey, Elena A. Minina, Boris Maček, Anders Hafrén, Tolga O. Bozkurt, Mary Beth Mudgett, Frederik Börnke, Daniel Hofius, Şuayib Üstün
Abstract
Beyond its role in cellular homeostasis, autophagy plays anti- and promicrobial roles in host-microbe interactions, both in animals and plants. One prominent role of antimicrobial autophagy is to degrade intracellular pathogens or microbial molecules, in a process termed xenophagy. Consequently, microbes evolved mechanisms to hijack or modulate autophagy to escape elimination. Although well-described in animals, the extent to which xenophagy contributes to plant-bacteria interactions remains unknown. Here, we provide evidence that Xanthomonas campestris pv. vesicatoria (Xcv) suppresses host autophagy by utilizing type-III effector XopL. XopL interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection. Intriguingly, XopL is targeted for degradation by defense-related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery. Our results implicate plant antimicrobial autophagy in the depletion of a bacterial virulence factor and unravel an unprecedented pathogen strategy to counteract defense-related autophagy in plant-bacteria interactions.