Abstract
Autophagy is an evolutionarily conserved process that recycles damaged or unwanted cellular components, and has been linked to plant immunity. However, how autophagy contributes to plant immunity is unknown. Here we reported that the plant autophagic machinery targets the virulence factor βC1 of Cotton leaf curl Multan virus (CLCuMuV) for degradation through its interaction with the key autophagy protein ATG8. A V32A mutation in βC1 abolished its interaction with NbATG8f, and virus carrying βC1V32A showed increased symptoms and viral DNA accumulation in plants. Furthermore, silencing of autophagy-related genes ATG5 and ATG7 reduced plant resistance to the DNA viruses CLCuMuV, Tomato yellow leaf curl virus, and Tomato yellow leaf curl China virus, whereas activating autophagy by silencing GAPC genes enhanced plant resistance to viral infection. Thus, autophagy represents a novel anti-pathogenic mechanism that plays an important role in antiviral immunity in plants.
Highlights
Plants have evolved various defense mechanisms to combat plant pathogens, including viruses
Since the V32A point mutation eliminates the interaction of bC1 with NbATG8f, these results suggest that the interaction of bC1 with NbATG8 is essential for the antiviral defense mechanism of autophagy against Cotton leaf curl Multan virus (CLCuMuV) infection
We show that geminivirus CLCuMuV infection activates autophagy and that autophagy targets the virulence protein bC1 for degradation
Summary
Plants have evolved various defense mechanisms to combat plant pathogens, including viruses. The activation of R gene-mediated resistance triggers a rapid defense response that often includes localized programmed cell death, known as the hypersensitive response (HR). The role of autophagy in plant defense responses against the bacterial pathogen Pseudomonas syringae DC3000 is controversial (Patel and Dinesh-Kumar, 2008; Hofius et al, 2009; Lenz et al, 2011). It is unclear how autophagy links plant immunity in these studies
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