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17Many of the world's most serious crop diseases are caused by hemibiotrophic fungi. These 18 pathogens have evolved the ability to colonize living plant cells, suppressing plant immunity 19 responses, before switching to necrotrophic growth, in which host cells die, providing the energy to 20 fuel sporulation and spread of the fungus. How hemibiotrophic pathogens switch between these two 21 lifestyles remains poorly understood. Here, we report that the devastating rice blast fungus, 22 Magnaporthe oryzae, manipulates host cellular pH to regulate hemibiotrophy. During infection by 23 M. oryzae, host plant cells are alkalinized to pH 7.8 during biotrophic growth, but later acidified to 24 pH 6.5 during necrotrophy. Using a forward genetic screen, we identified alkaline-sensitive mutants 25 of M. oryzae that were blocked in biotrophic proliferation and impaired in induction of host cell 26 acidification and necrotrophy. These mutants defined components of the PacC-dependent ambient 27 pH signal transduction pathway in M. oryzae. We report that PacC exists as a full-length repressor, 28 PacC 559 , and a truncated transcriptional activator, PacC 222 , which localize to the fungal nucleus 29 during biotrophic growth and to the cytoplasm during necrotrophy. During biotrophy, PacC 222 30 directly activates genes associated with nutrient acquisition and fungal virulence, while PacC 559 31 represses genes associated with saprophytic mycelial growth and sporulation, which are subsequently 32 de-repressed during necrotrophy. When considered together, our results indicate that temporal 33 regulation of hemibiotrophy by M. oryzae requires PacC-dependent sensing and manipulation of host 34 cellular pH.

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