Rice blast pathogen effector AvrPib compromises disease resistance by targeting Raf-like protein kinase OsMAPKKK72 to inhibit MAPK signaling.

Phytopathogens, such as the rice blast fungus Magnaporthe oryzae, suppress plant immunity for reproduction by secreting effectors into plant cells. The M. oryzae effector AvrPib is known to be recognized by Pib, an intracellular nucleotide-binding, leucine-rich repeat receptor (NLR), in rice. However, how AvrPib manipulates blast resistance and its potential targets in rice remains unclear. In this study, we showed that AvrPib interacts with the rice MAP KINASE KINASE KINASE 72 (OsMAPKKK72), a previously uncharacterized Raf-like MAPKKK. The osmapkkk72 mutant shows enhanced susceptibility to the M. oryzae strain Guy11 and reduced mitogen-activated protein kinase (MAPK) activation after treatment with chitin. Furthermore, OsMAPKKK72 interacts with MAP KINASE KINASE 9 (OsMKK9) and increases the interaction between OsMKK9 and OsMPK3/6. Accordingly, OsMKK9 positively regulates rice blast resistance and increases MAPK activation in an OsMAPKKK72-dependent manner following chitin treatment in rice, suggesting that OsMAPKKK72 may serve as a scaffold in the MAPK cascade. AvrPib inhibits the interaction between OsMAPKKK72 and OsMKK9, leading to reduced MAPK activation, which is mediated by OsMKK9. Taken together, our results reveal the critical roles of OsMAPKKK72 in blast resistance and uncover a mechanism wherein AvrPib suppresses rice blast resistance by interference with MAPK activation by targeting a key component in the MAPK cascade.