Rac1 Is Required for Pathogenicity and Chm1-Dependent Conidiogenesis in Rice Fungal Pathogen Magnaporthe grisea

• DOI: 10.1371/journal.ppat.1000202
• Publication Date: 2008-11-13T22:39:26Z
• Authors: Jisheng Chen; Wu Zheng; Shiqin Zheng; Dongmei Zhang; Weijian Sang; Xiao Chen; Guangpu Li; Guodong Lu; Zonghua Wang
• Keywords: Conidiation; Magnaporthe; Appressorium; Fungal protein

Rac1 is a small GTPase involved in actin cytoskeleton organization and polarized cell growth many organisms. In this study, we investigate the biological function of MgRac1, homolog Magnaporthe grisea. The Mgrac1 deletion mutants are defective conidial production. Among few conidia generated, they malformed appressorial formation consequently lose pathogenicity. Genetic complementation with native MgRac1 fully recovers all these phenotypes. Consistently, expression dominant negative allele exhibits same defect as mutants, while constitutively active can induce abnormally large defects infection-related growth. Furthermore, show interactions between its effectors, including PAK kinase Chm1 NADPH oxidases (Nox1 Nox2), by yeast two-hybrid assay. While Nox proteins important for pathogenicity, MgRac1-Chm1 interaction responsible conidiogenesis. A chm1 mutant, which Rac1-binding PBD domain removed, restores conidiation but do not develop appressoria normally pathogenic to rice plants. Our data suggest that pathway conidiogenesis, additional pathways, pathway, necessary