Transcriptomic reprogramming in a susceptible Phaseolus vulgaris L. variety during Pseudomonas syringae attack: The key role of homogalacturonan methylation
The susceptibility of common bean varieties to Pseudomonas syringae pv. phaseolicola (Pph) has been well-documented. However, the molecular mechanism that drives this susceptibility has not been clarified yet. In an attempt to understand this process, 15-day-old common bean plants, variety rinon, were infected with Pph to analyze the transcriptomic changes during the first steps of the infection (at 2 and 9 h). RNA-seq analysis showed an upregulation of defense-and signaling-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, suggesting that Pph could produce/induce changes in the CW. 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. From all HG-related genes modulated by the infection, 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 its PME inhibitory activity was demonstrated. Therefore, PvPMEI3 seems to be a good candidate to play a key role in Pph infection. This premise was supported by the analysis of Arabidopsis pmei3 mutant, which showed susceptibility to Pph, in contrast to resistant Col-0 control plants. 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 neither maintained during the necessary time, nor are deep enough to block the action of the pathogen, facilitating the well-known susceptibility of rinon variety to Pph.