Botany and Plant Pathology Seminar Series
Speaker: Dr. Richard Wilson - Department of Plant Pathology - University of Nebraska
Topic: Feeding frenzy: Mechanisms of in planta nutrient utilization during infection by the rice blast fungus
When: Wednesday, October 03, 2012 at 3:30 pm in WSLR 116
Abstract:

Rice contributes 23 percent of the calories consumed worldwide, but each year 10 to 30 percent of the global rice harvest – enough to feed 60 million people – is lost to rice blast disease. To infect rice, the filamentous fungus Magnaporthe oryzea has distinct morphogenetic stages that allow it to breach the surface of the host leaf and invade the plant tissue. How the fungus monitors the transition from the nutrient-free surface to the nutrient-rich interior of the leaf, what controls the genetic reprogramming necessary to produce infectious hyphae, and how it acquires nutrient during in planta growth is poorly understood. Our work has shown that M. oryzae’s trehalose-6-phosphate synthase 1 enzyme (Tps1) integrates carbon and nitrogen metabolism in the fungal cell to regulate virulence via a novel NADPH-dependent genetic switch. Tps1, in response to glucose sensing, is required for the production of NADPH in the oxidative pentose phosphate pathway and is essential for pathogenicity. Loss of Tps1 function results in Dtps1 strains that can form functional appressoria and penetrate the rice surface but fail to grow beyond the first infected cell. This impaired invasive growth of Dtps1 strains is due to loss of glucose sensing, inactivation of the NADPH-dependent genetic switch, and the concomitant activation of alternative carbon source utilization pathways in the presence of glucose resulting in impaired carbon assimilation. Moreover, NADPH-requiring processes such as reductive biosynthesis and antioxidation systems are shut down in Dtps1 strains. Consequently, Dtps1 strains are also defective in secondary metabolite production and are sensitive to oxidative stress compared to wild type parental strains. Taken together, I discuss here how, using classical and high-throughput reverse genetics, we are exploring the dynamics of this NADPH-dependent genetic switch to understand how NADPH production and depletion is balanced in the cell, how crucial NADPH-requiring processes are regulated by the availability of NADPH, and how these processes impact the ability of the fungus to cause disease.

 

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