DspA/E-triggered non-host resistance against E. amylovora depends on the Arabidopsis GLYCOLATE OXIDASE 2 gene
2022
Launay, Alban | Jolivet, Sylvie | Cléme, Gilles | Zarattini, Marco | Dellero, Younes | Le Hir, Rozenn | Jossier, Mathieu | Hodges, Michael | Expert, Dominique | Fagard, Mathilde
International audience
Show more [+] Less [-]English. DspA/E is a type three effector injected by the pathogenic bacterium Erwinia amylovorainside plant cells. In non-host Arabidopsis thaliana, DspA/E inhibits seed germination, root growth,de novo protein synthesis and triggers localized cell death. To better understand the mechanismsinvolved, we performed EMS mutagenesis on a transgenic line, 13-1-2, containing an inducible dspA/Egene. We identified three suppressor mutants, two of which belonged to the same complementationgroup. Both were resistant to the toxic effects of DspA/E. Metabolome analysis showed that the 13-1-2line was depleted in metabolites of the TCA cycle and accumulated metabolites associated with celldeath and defense. TCA cycle and cell-death associated metabolite levels were respectively increasedand reduced in both suppressor mutants compared to the 13-1-2 line. Whole genome sequencingindicated that both suppressor mutants displayed missense mutations in conserved residues ofGlycolate oxidase 2 (GOX2), a photorespiratory enzyme that we confirmed to be localized in theperoxisome. Leaf GOX activity increased in leaves infected with E. amylovora in a DspA/E-dependentmanner. Moreover, the gox2-2 KO mutant was more sensitive to E. amylovora infection and displayedreduced JA-signaling. Our results point to a role for glycolate oxidase in type II non-host resistanceand to the importance of central metabolic functions in controlling growth/defense balance.
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