RT Journal Article
SR Electronic
T1 Self-ubiquitination of a pathogen type-III effector traps and blocks the autophagy machinery to promote disease
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.03.17.435853
DO 10.1101/2021.03.17.435853
A1 Jia Xuan Leong
A1 Margot Raffeiner
A1 Daniela Spinti
A1 Gautier Langin
A1 Mirita Franz-Wachtel
A1 Andrew R. Guzman
A1 Jung-Gun Kim
A1 Pooja Pandey
A1 Alyona E. Minina
A1 Boris Macek
A1 Anders Hafrén
A1 Tolga O. Bozkurt
A1 Mary Beth Mudgett
A1 Frederik Börnke
A1 Daniel Hofius
A1 Suayib Üstün
YR 2021
UL http://biorxiv.org/content/early/2021/03/24/2021.03.17.435853.abstract
AB Beyond its role in cellular homeostasis, autophagy is considered to play anti- and pro-microbial roles in host-microbe interactions, both in animals and plants. One of the prominent roles of anti-microbial autophagy in animals 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. However, the extent to which xenophagy contributes to plant-bacteria interactions remains unknown. Here, we provide evidence that NBR1/Joka2-dependent selective autophagy functions in plant defence by degrading the bacterial type-III effector (T3E) XopL from Xanthomonas campestris pv. vesicatoria (Xcv). We show how XopL associates with the autophagy machinery and undergoes self-ubiquitination, subsequently triggering its own degradation by NBR1/Joka2-mediated selective autophagy. Intriguingly, Xcv is also able to suppress autophagy in a T3E-dependent manner by utilizing the same T3E XopL that interacts and degrades the autophagy component SH3P2 via its E3 ligase activity. Thus, XopL is able to escape its own degradation and promote pathogenicity of Xcv by inhibiting autophagy through SH3P2 depletion. Together, we reveal a novel phenomenon how NBR1/Joka2 contributes to anti-bacterial autophagy and provide a unique mechanism how a T3E undergoes self-modification to act as a bait to trap host cellular degradation machineries.Significant statement Autophagy has anti- and pro-microbial roles in host-microbe interactions. Its anti-microbial role is derived from its ability to degrade intracellular pathogens, termed “xenophagy”. The contribution of xenophagy to host-bacteria interactions in plants and its substrates remains elusive. Here, we reveal that NEIGHBOR OF BRCA1 (NBR1)-mediated autophagy has an anti-microbial role towards bacteria by degrading the type-III effector (T3E) XopL from Xanthomonas campestris pv. vesicatoria (Xcv). We unveil that the same T3E is able to perturb autophagy to escape its own degradation and to boost bacterial virulence. These findings highlight a novel role of xenophagy that is conserved across kingdoms and we offer new perspectives on how T3Es undergo self-modification to trap host cellular degradation pathways.Competing Interest StatementThe authors have declared no competing interest.