Unravelling the key steps impairing the metabolic state of Xanthomonas cells undergoing programmed cell death.

Abstract

Programmed cell death (PCD) has been reported in Xanthomonas axonopodis pv. glycines (Xag) wild type earlier and was indirectly shown to be induced by metabolic stress; however, deciphering the key proteins regulating the metabolic stress remained unrevealed. In this study, transcriptomic and proteomic analyses were performed to investigate the prominent pathways, having a role in the induction of metabolic stress in Xag cells undergoing PCD. A comprehensive analysis of transcriptome and proteome data revealed the major involvement of metabolic pathways related to branched chain amino acid degradation, such as acyl-CoA dehydrogenase and energy-yielding, ubiquinol:cytochrome c oxidoreductase complex, in Xag cells undergoing PCD. Consequently, oxidative stress response genes showed major upregulation in Xag cells in PCD-inducing medium; however, no such upregulation was observed at the protein level, indicative of depleted protein levels under excessive stress conditions. Activation of stress response and DNA repair proteins was also observed in Xag cells grown in PCD-inducing medium, which is indicative of excessive cellular damage. Thus, the findings indicate that programmed cell death in Xag is an outcome of metabolic stress in nutrient condition not suitable for a plant pathogen like Xanthomonas, which is more acclimatised with altogether a different nutritional requirement predominantly having an enriched carbohydrate source.