Deciphering the role of Arabidopsis thaliana heterotrimeric G protein in induced resistance against necrotrophic fungi


Abstract: Arabidopsis heterotrimeric G protein is required for an efficient defence response against different types of pathogens, including necrotrophic fungi such as Plectosphaerella cucumerina (PcBMM). Null mutants in the Gβ subunit (agb1) exhibit enhanced susceptibility to this pathogen, while mutants in the Gα subunit (gpa1) display a resistance phenotype. We have demonstrated that the agg1 agg2 double mutant is as susceptible as agb1 plants to PcBMM. To elucidate the molecular mechanism underlying the heterotrimeric G protein-mediated resistance, we performed a comparative transcriptomic analysis of agb1-1 mutant and wild-type plants upon inoculation with P. cucumerina. This analysis, together with metabolomic studies, demonstrated that G protein-mediated resistance was independent from the salicylic acid (SA)-, jasmonic acid (JA)-, ethylene (ET)-, abscisic acid (ABA)- or tryptophan-derived metabolites defensive signalling, as these pathways required for resistance to necrotrophs were not impaired in agb1-1 and agg1 agg2 plants. Notably, in agb1-1 transcriptome we found an overrepresentation of misregulated genes related with cell wall functions, which showed a similar expression pattern in agg1 agg2 plants. Biochemical analyses of cell walls from G-protein mutants and wild-type plants revealed that xylose content was lower in agb1 and agg1 agg2 mutants that in wild-type plants. These data suggest a canonical functionality of the Gβ and Gγ1/γ2 subunits in the control of Arabidopsis immune responses and cell wall composition, being this last critical for resistance to necrotrophic fungal pathogens. Genetic interactions with other regulatory genes required for defence against necrotrophic fungi have been analyzed in order to unravel the complex network for Arabidopsis G-protein defence signalling pathway. In line with this, some suppressors of agb1 susceptibility mutants (sgb) have been identified with different levels of resistance to PcBMM, that restore the agb1-immune deficient responses to wild-type levels.

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