The ArabidopsisRESURRECTION1Gene Regulates a Novel Antagonistic Interaction in Plant Defense to Biotrophs and Necrotrophs

Abstract

We report a role for the Arabidopsis (Arabidopsis thaliana) RESURRECTION1 (RST1) gene in plant defense. The rst1 mutant exhibits enhanced susceptibility to the biotrophic fungal pathogen Erysiphe cichoracearum but enhanced resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola. RST1 encodes a novel protein that localizes to the plasma membrane and is predicted to contain 11 transmembrane domains. Disease responses in rst1 correlate with higher levels of jasmonic acid (JA) and increased basal and B. cinerea-induced expression of the plant defensin PDF1.2 gene but reduced E. cichoracearum-inducible salicylic acid levels and expression of pathogenesis-related genes PR1 and PR2. These results are consistent with rst1's varied resistance and susceptibility to pathogens of different life styles. Cuticular lipids, both cutin monomers and cuticular waxes, on rst1 leaves were significantly elevated, indicating a role for RST1 in the suppression of leaf cuticle lipid synthesis. The rst1 cuticle exhibits normal permeability, however, indicating that the disease responses of rst1 are not due to changes in this cuticle property. Double mutant analysis revealed that the coi1 mutation (causing defective JA signaling) is completely epistatic to rst1, whereas the ein2 mutation (causing defective ethylene signaling) is partially epistatic to rst1, for resistance to B. cinerea. The rst1 mutation thus defines a unique combination of disease responses to biotrophic and necrotrophic fungi in that it antagonizes salicylic acid-dependent defense and enhances JA-mediated defense through a mechanism that also controls cuticle synthesis.

Overexpression of a LAM Domain Containing RNA-Binding Protein LARPIc Induces Precocious Leaf Senescence in Arabidopsis

“…Thus, we examined the expression levels of several defense-related genes by RT-PCR. Pathogenesisrelated (PR) genes PR1 and PR2 are SA pathway defense genes (Mang et al, 2009). Phytoalexin deficient 4 (PAD4) and Enhanced Disease Resistance 1 (EDS1) act upstream from SA biosynthesis but are also induced by SA (Rustérucci et al, 2001).…”

Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

“…The Arabidopsis glycosylphosphatidylinositol-anchored lipid transfer protein (ltpg1) mutant shows increased susceptibility to A. brassicicola attributed to changes in cuticle composition and structure further confi rming the link between altered cuticles and resistance to necrotrophic fungi (Lee et al, 2009b). In the case of rst1, increased resistance to B. cinerea and A. brassicicola is accompanied with susceptibility to the biotrophic fungal pathogen Erysiphe cichoracearum (Mang et al, 2009). Mutation in RST1, encoding a transmembrane protein of unknown biochemical function, leads to increased cutin monomers on the leaf surface without altered permeability.…”

“…This, coupled with an increased cuticle permeability that allows easier diffusion of defense signals to the infection site, is hypothesized to promote resistance (Bessire et al, 2007b; Chassot et al, 2007). However, mutant comparisons indicate that the degree of permeability does not directly correlate with level of resistance and is unaffected in rst1 (Mang et al, 2009;Voisin et al, 2009). It was also suggested that mutant plants compensate the functional disorder of the cuticle by reinforcing their defenses thereby enhancing resistance independent of the changes in actual cuticle composition (Voisin et al, 2009).…”

“…Interestingly, this resistance is specifi c to B. cinerea as plant responses to P. cucumerina, A. brassicicola, and S. sclerotiorum were unaltered (Chassot et al, 2007). Mutations in LACERATA (LCR), FIDDLEHEAD (FDH), BODYGUARD (BDG), LACS2 (BRE1) and RESURRECTION1 (RST1) also result in alter cuticle development and enhanced resistance to B. cinerea (Kurdyukov et al, 2006; Bessire et al, 2007b; Chassot et al, 2007;Mang et al, 2009;Voisin et al, 2009). In some of these cases, the altered cuticle composition was hypothesized to facilitate faster perception of fungal elicitors.…”

“…Shifts in cellular status and/or intracellular signaling from pathogen-triggered oscillations have the potential to serve at DAMPs upon host-recognition (Nurnberger et al, 2004; Lotze et al, 2007; Tor et al, 2009). Cyclic nucleotide-gated ion channel (CNGCs) facilitate increases in cytosolic calcium ion concentrations suffi cient for activation of signal transduction pathways required for innate defense responses (Lecourieux et al, 2006;Ma et al, 2009). Host perception of altered CNGC function may contribute to activation of defense during necrotrophic infection.…”