rac1 is required for pathogenicity and chm1-dependent conidiogenesis in rice fungal pathogen magnaporthe grisea需要rac1致病性和chm1-dependent conidiogenesis在水稻稻瘟病菌真菌病原体.pdfVIP

Rac1 Is Required for Pathogenicity and Chm1-Dependent Conidiogenesis in Rice Fungal Pathogen Magnaporthe grisea 1,2 1,3¤ 3 2 2 3 Jisheng Chen , Wu Zheng , Shiqin Zheng , Dongmei Zhang , Weijian Sang , Xiao Chen , Guangpu Li4,5, Guodong Lu1,3, Zonghua Wang1,2,3* 1 Key Laboratory of Biopesticide and Chemistry Biology, Ministry of Education, Fujian Agriculture and Forestry University, Fuzhou, China, 2 The School of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, China, 3 Plant Protection College, Fujian Agriculture and Forestry University, Fuzhou, China, 4 Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America, 5 The School of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, China Abstract Rac1 is a small GTPase involved in actin cytoskeleton organization and polarized cell growth in many organisms. In this study, we investigate the biological function of MgRac1, a Rac1 homolog in Magnaporthe grisea. The Mgrac1 deletion mutants are defective in conidial production. Among the few conidia generated, they are malformed and defective in appressorial formation and consequently lose pathogenicity. Genetic complementation with native MgRac1 fully recovers all these defective phenotypes. Consistently, expression of a dominant negative allele of MgRac1 exhibits the same defect as the deletion mutants, while expression of a constitutively active allele of MgRac1 can induce abnormally large conidia with defects in infection-related growth. Furthermore, we show the interactions between MgRac1 and its effectors, including the PAK kinase Chm1 and NADPH oxidase