Hofius, D. | Search bioRxiv

bioRxiv2021

Turnip crinkle virus targets host ATG8 proteins to attenuate antiviral autophagy

Autophagy has emerged as a central player in plant virus disease and resistance. In this study we have addressed the potential roles of autophagy in Turnip crinkle virus (TCV) infection. We found that autophagy attenuates disease severity and contributes to resistance against TCV by limiting virus accumulation. These autophagy-dependent disease phenotypes intensify further when combined with defects in RNA silencing, suggesting that these two major defence pathways are largely uncoupled in TCV disease. Intriguingly, as a counterdefence, TCV employs the viral silencing suppressor protein P38 to suppress antiviral autophagy, likely by directly sequestering ATG8 proteins. This strategy appears to be novel for plant viruses, yet resembles mechanisms described for other pathogen classes. Together, these results broaden our understanding of autophagy in plant virus disease, and strengthens our view of virus-specific adaptation to the autophagy pathway.

plant biology↗

bioRxiv2021

Self-ubiquitination of a pathogen type-III effector traps and blocks the autophagy machinery to promote disease

Beyond its role in cellular homeostasis, autophagy plays anti- and pro-microbial roles in host-microbe interactions, both in animals and plants. One prominent role of anti-microbial 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 depletion of a bacterial virulence factor and unravels an unprecedented pathogen strategy to counteract defense-related autophagy.

plant biology↗

bioRxiv2020

Autophagic degradation of the Cucumber mosaic virus virulence factor 2b balances antiviral RNA silencing with proviral plant fitness and virus seed transmission

Autophagy is a conserved intracellular degradation pathway that has recently emerged as an integral part of plant responses to virus infection. The elucidated mechanisms of autophagy range from the selective degradation of viral components to a more general attenuation of disease symptoms. In addition, several viruses are able to manipulate the autophagy machinery and counteract autophagy-dependent resistance. Despite these findings, the complex interplay of autophagy activities, viral pathogenicity factors, and host defence pathways in disease development remains poorly understood. In the current study, we analysed the interaction between autophagy and Cucumber mosaic virus (CMV) in Arabidopsis thaliana. We show that autophagy is induced during CMV infection and promotes the turnover of the major CMV virulence protein and RNA silencing suppressor 2b. Intriguingly, 2b itself dampens plant autophagy. In accordance with 2b degradation, we found that autophagy provides resistance against CMV by reducing viral RNA accumulation in an RNA silencing-dependent manner. Moreover, autophagy and RNA silencing pathways contribute to plant longevity and fecundity of CMV infected plants in an additive manner, uncoupling it from resistance. In addition to reduced fecundity, autophagy-deficient plants also failed to support seed transmission of the virus. We propose that autophagy attenuates CMV virulence via 2b degradation and thereby increases both plant and virus fitness with a trade-off penalty arising from increased RNA silencing-mediated resistance. Author summaryThe capacity of plants to fight pathogenic viruses in order to survive and minimize damage relies on profound cellular reprogramming events. These include the synthesis of new as well as the degradation of pre-existing cellular components, together shifting cellular homeostasis towards a better tolerance of disease and fortification of antiviral defence mechanisms. Autophagy is a prominent and highly conserved cellular degradation pathway that supports plant stress resilience. Autophagy functions vary broadly and range from rather unspecific renewal of cytoplasm to highly selective degradation of a wide collection of specific substrates. Autophagy is well established to be involved during virus infections in animals, and its importance has also recently emerged in virus diseases of plants. However, we are still far from a comprehensive understanding of the complexity of autophagy activities in host-virus interactions and how autophagy pathway engineering could be applied against viruses. Here, we have analyzed one of the traditional model plant viruses, Cucumber mosaic virus (CMV), and its interactions with autophagy. Our study revealed that autophagy is tightly integrated into CMV disease, influencing processes from plant health to CMV epidemiology.

plant biology↗