A novel PMEI3 in common bean suggests a key role of pectin methylesterification in Pseudomonas resistance.

Abstract

The mechanisms that drives the common bean susceptibility against Pseudomonas syringae (Pph) has not been clarified yet. For this, 15-day-old common bean plants, variety riñón, were infected with Pph to analyze the transcriptomic changes at 2 and 9h post-infection. RNA-seq analysis showed an upregulation of genes involved in defense/signaling at 2h, most of them being downregulated at 9h, suggesting that Pph would inhibit the transcriptomic reprogramming of the plant. This trend was also observed in the modulation of 101 cell wall (CW)-related genes. CW composition changes at early stages of Pph infection were associated with homogalacturonan methylation and the formation of egg boxes. Among the CW genes modulated, a pectin methylesterase inhibitor 3 (PvPMEI3) gene, closely related to AtPMEI3, was detected. PvPMEI3 protein was located in the apoplast and its PME inhibitory activity was demonstrated. PvPMEI3 seems to be a good candidate to play a key role in Pph infection, which was supported by the analysis of Arabidopsis pmei3 mutant, that showed susceptibility to Pph, in contrast to resistant Col-0 plants. All these results point to a key role of the pectin methylesterification degree affecting host resistance to Pph during the first steps of the attack.