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Abstract

Sclerotinia sclerotiorum is a devastating necrotrophic fungus with a broad host range, infecting hundreds of plant species, including many economically important crops. Despite its significant agricultural impact, the molecular mechanisms that control its developmental processes and virulence are still not well defined. To better understand these mechanisms, a forward genetic screen was performed, which led to the identification of six UV-induced mutants harboring loss-of-function mutations in the autophagy-related genes SsATG1, SsATG2, SsATG4, SsATG5, SsATG9, and SsATG26. Functional validation through targeted gene deletions revealed that each of these ATG genes is essential for normal sclerotia formation. Although the overall morphology of appressoria remained largely unaffected, the mutants exhibited varying levels of impairment in vegetative growth and pathogenicity. Autophagic activity was further examined using the GFP–ATG8 reporter system, which demonstrated dynamic changes in autophagosome formation during development of sclerotia. The reduced or absent autophagic flux in mutant strains correlated with their inability to produce mature sclerotia and their attenuated virulence, emphasizing the importance of autophagy in fungal differentiation and infection. These results indicate that both macroautophagy and pexophagy play fundamental roles in nutrient recycling and energy allocation required for sclerotia maturation. Together, this study establishes a clear link between the autophagy machinery and the developmental and pathogenic processes of S. sclerotiorum. It provides a foundation for future investigations into specific cellular targets and regulatory pathways through which autophagy influences fungal virulence. Elucidating these mechanisms may ultimately contribute to the identification of novel molecular targets for controlling diseases caused by this highly destructive pathogen.