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.

中文翻译：

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揭示损害黄单胞菌细胞程序性细胞死亡代谢状态的关键步骤

摘要

据报道，Xanthomonas axonopodis pv. 存在程序性细胞死亡 (PCD)。甘氨酸 (Xag) 野生型较早，并被间接证明是由代谢应激诱导的；然而，破译调节代谢应激的关键蛋白质仍未揭晓。在这项研究中，进行了转录组和蛋白质组分析，以研究在经历 PCD 的 Xag 细胞中诱导代谢应激中发挥作用的重要途径。对转录组和蛋白质组数据的综合分析揭示了在经历 PCD 的 Xag 细胞中与支链氨基酸降解相关的代谢途径的主要参与，例如酰基辅酶 A 脱氢酶和产生能量的泛醇：细胞色素 c 氧化还原酶复合物。因此，氧化应激反应基因在 PCD 诱导培养基中的 Xag 细胞中表现出大幅上调；然而，在蛋白质水平上没有观察到这种上调，表明过度应激条件下蛋白质水平下降。在 PCD 诱导培养基中生长的 Xag 细胞中也观察到应激反应和 DNA 修复蛋白的激活，这表明细胞损伤过度。因此，研究结果表明，Xag 中的程序性细胞死亡是不适合黄单胞菌等植物病原体的营养条件下代谢应激的结果，黄单胞菌更能适应主要具有丰富碳水化合物来源的完全不同的营养需求。