SsdchA is a novel secretory cellobiohydrolase driving pathogenicity in Sclerotinia sclerotiorum
作者机构:Integrative Science Center of Germplasm Creation in Western China(Chongqing)Science CityCollege of Agronomy and BiotechnologySouthwest UniversityChongqing 400715China Academy of Agricultural SciencesSouthwest UniversityChongqing 400715China Engineering Research Center of South Upland AgricultureMinistry of EducationChongqing 400715China College of Plant ProtectionSouthwest UniversityChongqing 400715China
出 版 物:《The Crop Journal》 (作物学报(英文版))
年 卷 期:2024年第12卷第2期
页 面:493-502页
核心收录:
学科分类:09[农学] 0904[农学-植物保护] 090401[农学-植物病理学]
基 金:financially supported by the National Nature Science Foundation of China (32372077) the Project of Chongqing Science and Technology Commission (CSTB2023NSCQ-MSX0355) the Fundamental Research Funds for the Central Universities (SWU120075)
主 题:Cellobiohydrolase Cellulose Pathogenicity Sclerotinia sclerotiorum Secretory protein SsdchA
摘 要:The necrotrophic fungus, Sclerotinia sclerotiorum, employs an array of cell wall-degrading enzymes(CWDEs), including cellulase, to dismantle host cell walls. However, the molecular mechanisms through which S. sclerotiorum degrades cellulose remain elusive. Here, we unveil a novel secretory cellobiohydrolase, SsdchA, characterized by a signal peptide and a Glyco_hydro_7(GH7) domain. SsdchA exhibits a robust expression of during early infection stages. Interestingly, colony morphology and growth rates remain unaffected across the wild-type, SsdchA deletion strains and SsdchA overexpression strains on potato dextrose agar(PDA) medium. Nevertheless, the pathogenicity and cellobiohydrolase activity decreased in the SsdchA deletion strains, but enhanced in the SsdchA overexpression strains. Moreover,the heterologous expression of SsdchA in Arabidopsis thaliana leads to reduced cellulose content and heightened susceptibility to S. sclerotiorum. Collectively, our data underscore the pivotal role of the novel cellobiohydrolase SsdchA in the pathogenicity of S. sclerotiorum.