(2008). Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes. Autophagy: Vol. 4, No. 2, pp. 151-175.

The Woronin body is a peroxisome-derived dense-core vesicle that is specific to several genera of filamentous ascomycetes, where it has been shown to seal septal pores in response to cellular damage. The Hexagonal peroxisome (Hex1) protein was recently identified as a major constituent of the Woronin body and shown to be responsible for self-assembly of the dense core of this organelle. Using a mutation in the Magnaporthe grisea HEX1 ortholog, we define a dual and essential function for Woronin bodies during the pathogenic phase of the rice blast fungus. We show that the Woronin body is initially required for proper development and function of appressoria (infection structures) and subsequently necessary for survival of infectious fungal hyphae during invasive growth and host colonization. Fungal mycelia lacking HEX1 function were unable to survive nitrogen starvation in vitro, suggesting that in planta growth defects are a consequence of the mutant's inability to cope with nutritional stress. Thus, Woronin body function provides the blast fungus with an important defense against the antagonistic and nutrient-limiting environment encountered within the host plant.

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.