Alteration of cell wall xylan acetylation triggers defense responses that counterbalance the immune deficiencies of plants impaired in the β‐subunit of the heterotrimeric G‐protein

Abstract

[EN] Arabidopsis heterotrimeric G-protein complex modulates pathogen-associated molecular pattern-triggeredimmunity (PTI) and disease resistance responses to different types of pathogens. It also plays a role in plantcell wall integrity as mutants impaired in the Gb-(agb1-2)orGc-subunits have an altered wall compositioncompared with wild-type plants. Here we performed a mutant screen to identify suppressors ofagb1-2(sgb) that restore susceptibility to pathogens to wild-type levels. Out of the foursgbmutants (sgb10–sgb13)identified,sgb11is a new mutant allele ofESKIMO1(ESK1), which encodes a plant-specific polysaccharideO-acetyltransferase involved in xylan acetylation. Null alleles (sgb11/esk1-7)ofESK1restore to wild-typelevels the enhanced susceptibility ofagb1-2to the necrotrophic fungusPlectosphaerella cucumerina BMM(PcBMM), but not to the bacteriumPseudomonas syringaepv.tomatoDC3000 or to the oomyceteHyaloper-onospora arabidopsidis. The enhanced resistance toPcBMMof theagb1-2 esk1-7double mutant was notthe result of the re-activation of deficient PTI responses inagb1-2. Alteration of cell wall xylan acetylationcaused byESK1impairment was accompanied by an enhanced accumulation of abscisic acid, the constitu-tive expression of genes encoding antibiotic peptides and enzymes involved in the biosynthesis of trypto-phan-derived metabolites, and the accumulation of disease resistance-related secondary metabolites anddifferent osmolites. Theseesk1-mediated responses counterbalance the defective PTI andPcBMMsuscepti-bility ofagb1-2plants, and explain the enhanced drought resistance ofesk1plants. These results suggestthat a deficient PTI-mediated resistance is partially compensated by the activation of specific cell-wall-trig-gered immune responses.