PAMP-responsive phosphoprotein MARK1 limits program cell death induction
H. NAKAGAMI (1), H. Matsui (2), Y. Nomura (3), M. Egusa (4), G. Hyon (3), H. Kaminaka (4), M. Trujillo (5), K. Shirasu (3) (1) RIKEN CSRS / Max Planck Institute for Plant Breeding Research, Japan; (2) RIKEN CSRS / Okayama University, Japan; (3) RIKEN CSRS, Japan; (4) Tottori University, Japan; (5) Leibniz Institute of Plant Biochemistry, Germany

Rapid cell death induction is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. By contrast, cell death can negatively impact disease resistance, as cells cannot further mount defense responses. Cell death is taken advantage of by necrotrophic pathogens which thrive on dead tissue. The poorly described cell death constraining system could allow plants to solve this conundrum. Here we show that pathogen-associated molecular pattern (PAMP)-responsive phosphoprotein MARK1 contributes to the containment of the hypersensitive response (HR) cell death caused by the avirulent bacterial pathogen in Arabidopsis thaliana. Moreover, MARK1 is required for PAMP-induced suppression of the fungal toxin fumonisin B1-triggered cell death. Inactivation of MARK1 does not result in spontaneous lesions, and the enhanced HR is independent of sid2 or rbohd, which are impaired in salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production, respectively. Importantly, mark1 T-DNA insertion mutants display enhanced susceptibility to the virulent hemi-biotrophic bacterial pathogen. These findings pointing to the existence and importance of SA and ROS independent cell death constraining mechanism that is modulated by PAMP-triggered immunity (PTI) as part of plant immune system.

Abstract Number: P17-575
Session Type: Poster