Journal article
M. J. Kershaw, M. Basiewicz, D. Soanes, Xia Yan, Lauren S. Ryder, M. Csukai, Míriam Osés-Ruiz, B. Valent, N. Talbot
Genetics, 2018
Genetics, 2018
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DOI
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APA
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Kershaw, M. J., Basiewicz, M., Soanes, D., Yan, X., Ryder, L. S., Csukai, M., … Talbot, N. (2018). Conidial Morphogenesis and Septin-Mediated Plant Infection Require Smo1, a Ras GTPase-Activating Protein in Magnaporthe oryzae. Genetics.
Chicago/Turabian
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Kershaw, M. J., M. Basiewicz, D. Soanes, Xia Yan, Lauren S. Ryder, M. Csukai, Míriam Osés-Ruiz, B. Valent, and N. Talbot. “Conidial Morphogenesis and Septin-Mediated Plant Infection Require Smo1, a Ras GTPase-Activating Protein in Magnaporthe Oryzae.” Genetics (2018).
MLA
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Kershaw, M. J., et al. “Conidial Morphogenesis and Septin-Mediated Plant Infection Require Smo1, a Ras GTPase-Activating Protein in Magnaporthe Oryzae.” Genetics, 2018.
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@article{m2018a,
title = {Conidial Morphogenesis and Septin-Mediated Plant Infection Require Smo1, a Ras GTPase-Activating Protein in Magnaporthe oryzae},
year = {2018},
journal = {Genetics},
author = {Kershaw, M. J. and Basiewicz, M. and Soanes, D. and Yan, Xia and Ryder, Lauren S. and Csukai, M. and Osés-Ruiz, Míriam and Valent, B. and Talbot, N.}
}
Abstract
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 > 25 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 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, which regulates Ras signaling during infection-related development. Targeted deletion of SMO1 results in abnormal, nonadherent 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 the organization of microtubules and for septin-dependent remodeling of the F-actin cytoskeleton at the appressorium pore. Smo1 physically interacts with components of the Ras2 signaling complex, and a range of other signaling and cytoskeletal components, including the four core septins. SMO1 is therefore necessary for the regulation of RAS activation required for conidial morphogenesis and septin-mediated plant infection.