A Novel Chorismate Mutase Effector from the Necrotroph Fungal Phytopathogen Sclerotinia Sclerotiorum is a Functional Relative of an Effector from the Biotroph Ustilago Maydis
Conference Recording Feb 25, 2013
About the Speaker
Received his B.S. degree in Horticulture and his M.S. and Ph.D. degrees in Plant Pathology/Biochemistry from the University of Hawaii. In December 2005, Dr. Dickman was appointed Director of the Institute for Plant Genomics and Biotechnology at Texas A&M University where he is the Christine Richardson Professor in Agriculture. He is also the recipient of E.C. Stakman Award-2011 for excellence in plant pathology. He was recently named a Fellow of the American Association for the Advancement of Science (AAAS). Abstract
Plant associated fungi and oomycetes have adopted different lifestyles and strategies to achieve pathogenic success. Necrotrophic pathogens (e.g. Sclerotinia sclerotiorum-the focus of this preprosal) by definition, require dead host cells for nutrient acquisition. In contrast, biotrophic fungal growth occurs without disease symptoms and the integrity of the host plasma membrane is maintained as nutrient acquisition takes place. Hemibiotrophs have an early asymptomatic biotrophic phase that transitions into necrotrophy as evidenced by tissue damage and host cell death. Whereas resistance toward biotrophic pathogens is predominantly mediated by the recognition of pathogen effectors via R gene-encoded intracellular receptors, R gene-dependent resistance toward necrotrophic fungi has not been identified. This is not unexpected, as necrotrophs synthesize and deliver toxic metabolites that rapidly kill host cells. Accumulating evidence however, supports the idea that necrotrophic plant pathogens interact with their hosts in a more subtle manner than originally considered. Several lines of evidence show S. sclerotiorum growing through living plant tissue early during the infection process, suggesting that this fungus has a short biotrophic phase during pathogenic development. More recently, we have made an intriguing observation and obtained supportive experimental evidence that serves as the basis for this proposal. Ustilago maydis, the corn smut pathogen, and model biotroph, secretes an effector protein, encoding chorismate mutase (Cmu1) that is required for full virulence. Comparative studies indicated this gene was associated with biotrophs, several hemibiotrophs (with extended biotrophic phases) and nematodes, but is absent in all necrotrophs studied with the remarkable exception of S. sclerotiorum. S. sclerotiorum chorismate mutase (SsCM1) can heterodimerize with plant chorismate mutases. Gene replacement of SsCM1results in attenuated virulence, but normal fungal growth and development is unaffected. Our data indicates that SsCM1 functions as a bona fide secreted effector and raise several interesting questions regarding how a biotroph and necrotroph utilize the same biochemical activity to achieve pathogenic success. We hypothesize that during the early stages of infection S. sclerotiorum secretes an effector(s) that contributes to disease development.