Glucose-TOR signaling regulates cell cycle progression and autophagy during appressorium development by the rice blast fungus Magnaporthe oryzae
G. SUN (1), M. Marroquin-Guzman (1), R. Wilson (1) (1) Department of Plant Pathology, U.S.A.

Magnaporthe oryzae, the devastating rice blast fungus, accesses hosts by forming terminal plant-infecting cells, called appressoria, at the tips of germ tubes emerging from three-celled spores (conidia) on the nutrient-free leaf surface. Appressorial development is accompanied by a single round of mitosis followed by autophagic cell death of conidial nuclei. We recently showed that inactivation of the conserved target of rapamycin (TOR) signaling pathway is essential for appressorium formation, but how TOR controls this process is not known. Here, we show that a novel glucose-responsive gene, ABL1, is required to inhibit TOR function in the absence of glucose-signaling during appressorium formation.. Compared to wild type (WT), Dabl1 mutant strains undertook multiple rounds of mitosis in elongated germ tubes, formed few appressoria, and were abolished for autophagy. Treating germinating spores with glucose phenocopied the loss of ABL1 function in WT. Inactivating TOR in Dabl1 mutant strains, or in glucose-treated WT spores, restored appressorial differentiation by arresting mitosis at G1/G0 via an appressorium-inducing cell cycle pause at G2. We conclude that the glucose-ABL1-TOR signaling axis controls cell cycle progression, autophagy and the induction of appressorial development.  

Abstract Number: P7-213
Session Type: Poster