Transcriptomic reprogramming in a susceptiblePhaseolus vulgarisL. variety duringPseudomonas syringaeattack: The key role of homogalacturonan methylation

Abstract

The molecular mechanism that drives the resistance/susceptibility of common bean to Pseudomonas syringae pv. phaseolicola (Pph) has not been clarified yet. For this purpose, 15-day-old common bean plants, variety riñón, were infected with Pph to analyze the transcriptomic changes at 2 and 9 h. RNA-seq analysis showed an upregulation of defense-related genes 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. However, the changes in CW composition at early stages of Pph infection were related to homogalacturonan (HG) methylation and the formation of HG egg boxes. A common bean pectin methylesterase inhibitor 3 (PvPMEI3) gene - closely related to AtPMEI3 - was detected. In addition, PMEI3 protein was located in the apoplast and had inhibitory activity. Therefore, PvPMEI3 seems to be a good candidate to play a key role in infection, because Arabidopsis pmei3 mutant showed susceptibility to Pph. All these changes could be an attempt to reinforce the CW structure and thus, hinder the attack of the bacterium. However, these transcriptional and CW-remodeling processes are not deep enough to block the action of the pathogen.