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

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 Galpha(s)) 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 Galpha(i) 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.AlF(4)(-)-activated forms of MagA, MagB and MagC (a Galpha(II) subunit). Thus, Rgs1 serves as a negative regulator of all Galpha subunits in Magnaporthe and controls important developmental events during asexual and pathogenic development.