Mechanisms of adaptation to host rice cells by the blast fungus Magnaporthe oryzae

Rice blast disease is considered one of the most serious diseases of cultivated rice and is mediated by the causal agent, Magnaporthe oryzae. It is a hemi-biotroph that exhibits symptomless biotrophic growth for the first 4-5 days of infection of susceptible cultivars before becoming necrotrophic. To infect rice, the rice blast fungus 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 nutrients during biotrophic in planta growth is poorly understood. M. oryzae\u27s trehalose-6-phosphate synthase 1 (Tps1) enzyme integrates carbon and nitrogen metabolism in the fungal cell to regulate virulence via a novel NADPH-dependent genetic switch. Loss of Tps1 function results in Δ tps1 strains that can form functional appressoria and penetrate the rice surface but fail to grow beyond the first infected cell. Impaired invasive growth of Δtps1 strains is due to loss of glucose sensing, inactivation of the NADPH-dependent genetic switch, and altered carbon assimilation. Moreover, NADPH-requiring antioxidation systems are shut down in Δtps1 strains, rendering them hypersensitive to oxidative stress. Taken together, I discuss here how, using classical and high-throughput reverse genetics, I explored the dynamics of this critical NADPH-dependent genetic switch to understand how M. oryzae controls infectious hyphal development during biotrophy, how it responds to and acquires nutrients from the host, and how these processes are integrated to allow successful colonization of rice cells