P-340 - A FEEDBACK MECHANISM REGULATES THE PMK1 MITOGEN-ACTIVATED PROTEIN KINASE PATHWAY IN THE RICE BLAST FUNGUS

Rice blast disease destroys enough rice to feed 60 million people every year. The disease is caused by the fungus Magnaporthe oryzae, which invades hosts via a specialised cell called an appressorium. Deletion of a mitogen activated protein kinase (MAPK) encoding gene called Pathogenicity MAPK 1 (Pmk1) is well known to abrogate appressorium development. Pmk1 is activated by a MAPK kinase, Mst7, which is downstream of a MAPK kinase kinase, Mst11. The MAPK module triggers a signalling cascade regulating appressorium development and infection. In eukaryotes, this system is conserved and known to be regulated by phosphorylation. Recent phosphoproteomic analysis identified Pmk1-dependent phosphosites in Mst7, providing evidence Pmk1 putatively regulates its upstream components. We generated amino acid substitution mutations in MST7 S358, one such residue phosphorylated in a Pmk1-dependent manner. We then tested these mutants for appressorium development and infection-associated phenotypes. We report here that mutants of a Pmk1 dependent phosphosite in Mst7 show altered appressorium formation and virulence in infection assays. These results provide evidence that Pmk1 phosphorylation of upstream components of the MAPK pathway negatively regulate appressorium development and plant infection. This is consistent with operation of a phosphorylation-dependent feedback regulatory mechanism in the Pmk1 signalling cascade to tightly control appressorium development during plant infection.