Immune deficiencies of plants impaired in heterotrimeric G protein are counterbalanced by defense reponses triggered by alteration of cell wall xylan.
Immune deficiencies of plants impaired in heterotrimeric G protein are counterbalanced by defense reponses triggered by alteration of cell wall xylan
The plant heterotrimeric G protein complex is an essential component of Pathogen Associated Molecular Pattern-Triggered Immunity (PTI) and of plant disease resistance to several types of pathogens. It also plays a role in plant cell wall integrity as mutants impaired in the Gβ (agb1-2) or Gγ subunits have an altered wall composition compared to wild-type plants. In this article the “Plant innate Immunity and resistance to necrotrophic fungi” group of the CBGP (UPM-INIA)” found that the modification of the degree of xylan acetylation in plant cell walls, impairing Arabidopsis thaliana ESKIMO1 (ESK1) gene, activates PTI-independent resistance responses that counterbalance the hypersusceptibility to particular pathogens of plants lacking the heterotrimeric Gβ subunit. ESK1 inactivation is accompanied by an enhanced accumulation of abscisic acid, the constitutive expression of genes encoding antibiotic peptides and enzymes involved in the biosynthesis of tryptophan-derived metabolites, and the accumulation of disease resistance-related secondary metabolites and osmolites. The article data demonstrate that immune deficient response can be partially compensated by the activation of cell wall-triggered immunity that confers specific disease resistance, further supporting the relevance of the cell wall in the regulation of plant disease resistance.
In this article the CBGP (UPM-INIA) Plant Innate Immunity group has collaborated with researchers from the University of North Carolina (Chapel Hill, USA), the Royal Institute of Technology (KTH, Sweden), the University of Adelaide (Australia), and the enterprise Metabolon (NC, USA).
Cell wall-based immunity mediated by ESK1 impairment. In wild-type plants (left panel) PAMPs perception by PRR receptors and co-receptors leads to the activation of heterotrimeric G protein complex, which in turns modulate ROS production, MAPK phosphorylation and gene expression to positively activate PTI. In agb1-2 mutants (right panel) these responses are defective, but alterations in plant cell wall caused by esk1-7 mutation (agb1-2 esk1-7 plants) leads to the activation of cell wall-mediated DAMP-Triggered Immunity (DTI) responses, which overcompensate agb1-2 defective PTI responses