Taishi Hirase / Nara Institute of Science and Technology
Shigetaka Yasuda / Nara Institute of Science and Technology
Lionel Verdoucq / CNRS
Kohji Yamada / Tokushima University
Iris Finkemeier / University of Münster
Hirofumi Nakagami / MPIPZ
Sheng Yang He / Michigan State University
Christophe Maurel / CNRS
Yusuke Saijo / Nara Institute of Science and Technology
Plant-pathogen interactions are profoundly influenced by water availability, and often result in severe plant diseases under high humidity. The bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000 develops an aqueous leaf apoplast with type III secretion effectors (T3Es) for virulence promotion. However, whether and if so how plants directly resist against bacterial water acquisition is poorly understood. Here, we report a critical role for the plasma membrane intrinsic proteins (PIPs) in pattern triggered immunity to bacteria. In Arabidopsis thaliana, PIPs physically associate with the pattern recognition receptors (PRRs) FLS2 and PEPR1 for bacterial flagellin and endogenous Pep peptides, respectively. Remarkably, of the thirteen PIP members, dysfunction of one member permits an effector-less Pst strain to cause apoplastic water accumulation and enhanced proliferation. Genetic and biochemical evidence indicates that PIP phosphorylation in response to PRR activation leads to direct resistance against bacterial water soaking, possibly via enhanced water transport, and that the PRR-associated kinase BAK1 can mediate this PIP phosphorylation event. Conversely, Pst employs specific T3Es to intercept this novel PRR signaling output for water soaking. Our findings suggest that PIP phosphorylation by PRR complexes provides a basis for apoplastic water control during bacterial resistance.