RT Journal Article
SR Electronic
T1 <em>Magnaporthe oryzae SMO1</em> encodes a Ras GTPase-activating protein required for spore morphology, appressorium function and rice blast disease
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 388298
DO 10.1101/388298
A1 Michael J. Kershaw
A1 Magdalena Basiewicz
A1 Darren M. Soanes
A1 Xia Yan
A1 Lauren S. Ryder
A1 Michael Csukai
A1 Barbara Valent
A1 Nicholas J. Talbot
YR 2018
UL http://biorxiv.org/content/early/2018/08/08/388298.abstract
AB The pathogenic life cycle of the rice blast fungus Magnaporthe oryzae involves a series of morphogenetic changes, essential for its ability to cause disease. The smo mutation was identified more than twenty-five years ago and affects the shape and development of diverse cell types in M. oryzae, including conidia, appressoria and asci. All attempts to clone the SMO1 gene by map-based cloning and/or complementation, have failed over many years. Here, we report the identification of SMO1 by a combination of bulk segregant analysis and comparative genome analysis. SMO1 encodes a GTPase-activating protein (GAP), which regulates Ras signalling during infection-related development. Targeted deletion of SMO1 results in abnormal, non-adherent conidia, impaired in their production of spore tip mucilage. Smo1 mutants also develop smaller appressoria, with a severely reduced capacity to infect rice plants. SMO1 is necessary for organisation of microtubules and for septin-dependent remodelling of the F-actin cytoskeleton at the appressorium pore. Smo1 physically interacts with components of the Ras2 signaling complex, and a range of other signalling and cytoskeletal components, including the four core septins. SMO1 is therefore necessary for regulation of RAS activation required for conidial morphogenesis and septin-mediated plant infection.