Abstract

Sclerotinia sclerotiorum causes devastating diseases in many agriculturally important crops, including oilseed rape and sunflower. However, the mechanisms of Sclerotinia sclerotiorum pathogenesis remain poorly understood. In this study, we characterized a YML079-like cupin protein (SsYCP1) from Sclerotinia sclerotiorum. We showed that SsYCP1 is strongly expressed and secreted during Sclerotinia sclerotiorum infection. Sclerotinia sclerotiorum infection was promoted by SsYCP1 overexpression and inhibited by silencing this gene with synthetic double-stranded RNA. These results collectively indicate SsYCP1 as a putative effector protein that contributes to Sclerotinia sclerotiorum pathogenicity. These findings extend our understanding of effector-mediated Sclerotinia sclerotiorum pathogenesis and suggest a novel role for YML079-like cupin proteins in plant–pathogen interactions.

Highlights

  • Brassica napus is an important economic crop, and rapeseed oil is one of the world’s major edible oils

  • A previous study showed that 6% of S. sclerotiorum proteins (695 of 11,130) contain Signal peptides (SP) and lack predicted transmembrane domains (TM) [23], which could be potential effector proteins

  • S. sclerotiorum infection, whereas SsYCP1 silencing by synthetic double-stranded RNA suppressed S. sclerotiorum infection, demonstrating a positive role of SsYCP1 in S. sclerotiorum pathogenesis

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Summary

Introduction

Brassica napus is an important economic crop, and rapeseed oil is one of the world’s major edible oils. Sclerotinia disease, resulting from infection with Sclerotinia sclerotiorum, a necrotrophic ascomycete fungal pathogen, causes significant yield losses and quality reduction in B. napus [3,4]. Many researchers have been trying to develop new B. napus cultivars that are resistant to S. sclerotiorum through hybrid breeding. The progress is relatively slow, largely due to the lack of complete resistant genetic materials in Brassica species [3,5,6,7,8,9]. A more comprehensive and in-depth understanding of S. sclerotiorum pathogenesis might inspire a new strategy for Sclerotinia disease control

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