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(Homo)glutathione Depletion Modulates Host Gene Expression during the Symbiotic Interaction between Medicago truncatula and Sinorhizobium meliloti

机译:(同源)谷胱甘肽耗竭调节苜蓿苜蓿和苜蓿中华根瘤菌之间的共生相互作用过程中宿主基因表达。

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Under nitrogen-limiting conditions, legumes interact with symbiotic rhizobia to produce nitrogen-fixing root nodules. We have previously shown that glutathione and homoglutathione [(h)GSH] deficiencies impaired Medicago truncatula symbiosis efficiency, showing the importance of the low Mr thiols during the nodulation process in the model legume M. truncatula. In this study, the plant transcriptomic response to Sinorhizobium meliloti infection under (h)GSH depletion was investigated using cDNA-amplified fragment length polymorphism analysis. Among 6,149 expression tags monitored, 181 genes displayed significant differential expression between inoculated control and inoculated (h)GSH depleted roots. Quantitative reverse transcription polymerase chain reaction analysis confirmed the changes in mRNA levels. This transcriptomic analysis shows a down-regulation of genes involved in meristem formation and a modulation of the expression of stress-related genes in (h)GSH-depleted plants. Promoter-β-glucuronidase histochemical analysis showed that the putative MtPIP2 aquaporin might be up-regulated during nodule meristem formation and that this up-regulation is inhibited under (h)GSH depletion. (h)GSH depletion enhances the expression of salicylic acid (SA)-regulated genes after S. meliloti infection and the expression of SA-regulated genes after exogenous SA treatment. Modification of water transport and SA signaling pathway observed under (h)GSH deficiency contribute to explain how (h)GSH depletion alters the proper development of the symbiotic interaction.
机译:在限氮条件下,豆类与共生根瘤菌相互作用,产生固氮根瘤。先前我们已经表明,谷胱甘肽和高谷胱甘肽[(h)GSH]缺陷会损害Medi藜苜蓿的共生效率,这表明在豆科植物M. truncatula的结瘤过程中,低硫醇先生的重要性。在这项研究中,使用cDNA扩增的片段长度多态性分析研究了(h)GSH耗竭下对苜蓿中华根瘤菌感染的植物转录反应。在监测的6,149个表达标签中,有181个基因在接种的对照和接种的(h)GSH耗尽根之间显示出显着的差异表达。定量逆转录聚合酶链反应分析证实了mRNA水平的变化。这项转录组学分析显示,在(h)GSH耗尽的植物中,分生组织形成相关基因的表达下调,胁迫相关基因表达的调节。启动子-β-葡萄糖醛酸苷酶组织化学分析表明,假定的MtPIP2水通道蛋白可能在结节分生组织形成过程中被上调,并且在(h)GSH消耗下该上调受到抑制。 (h)GSH耗竭提高了苜蓿链球菌感染后水杨酸(SA)调控基因的表达以及外源SA处理后SA调控基因的表达。在(h)GSH缺乏下观察到的水运输和SA信号转导途径的改变有助于解释(h)GSH的消耗如何改变共生相互作用的适当发展。

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