Rgs1 regulates multiple Gα subunits in Magnaporthe pathogenesis, asexual growth and thigmotropism

Abstract

Regulators of G‐protein signaling (RGS proteins) negatively regulate heterotrimeric G‐protein cascades that enable eukaryotic cells to perceive and respond to external stimuli. The rice‐blast fungus Magnaporthe grisea forms specialized infection structures called appressoria in response to inductive surface cues. We isolated Magnaporthe RGS1 in a screen for mutants that form precocious appressoria on non‐inductive surfaces. We report that a thigmotropic cue is necessary for initiating appressoria and for accumulating cAMP. Similar to an RGS1 ‐deletion strain, magA G187S (RGS‐insensitive Gαs) and magA Q208L (GTPase‐dead) mutants accumulated excessive cAMP and elaborated appressoria on non‐inductive surfaces, suggesting that Rgs1 regulates MagA during pathogenesis. Rgs1 was also found to negatively regulate the Gαi subunit MagB during asexual development. Deficiency of MAGB suppressed the hyper‐conidiation defect in RGS1 ‐deletion strain, whereas magB G183S and magB Q204L mutants produced more conidia, similar to the RGS1 ‐deletion strain. Rgs1 physically interacted with GDP·AlF4−‐activated forms of MagA, MagB and MagC (a GαII subunit). Thus, Rgs1 serves as a negative regulator of all Gα subunits in Magnaporthe and controls important developmental events during asexual and pathogenic development.