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首页> 外文期刊>Journal of bacteriology >Mutations in rpoBC Suppress the Defects of a Sinorhizobium meliloti relA Mutant
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Mutations in rpoBC Suppress the Defects of a Sinorhizobium meliloti relA Mutant

机译:rpoBC中的突变抑制了苜蓿中华根瘤菌relA突变体的缺陷。

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The nitrogen-fixing symbiosis between Sinorhizobium meliloti and Medicago sativa requires complex physiological adaptation by both partners. One method by which bacteria coordinately control physiological adaptation is the stringent response, which is triggered by the presence of the nucleotide guanosine tetraphosphate (ppGpp). ppGpp, produced by the RelA enzyme, is thought to bind to and alter the ability of RNA polymerase (RNAP) to initiate and elongate transcription and affect the affinity of the core enzyme for various sigma factors. An S. meliloti relA mutant which cannot produce ppGpp was previously shown to be defective in the ability to form nodules. This mutant also overproduces a symbiotically necessary exopolysaccharide called succinoglycan (38). The work presented here encompasses the analysis of suppressor mutants, isolated from host plants, that suppress the symbiotic defects of the relA mutant. All suppressor mutations are extragenic and map to either rpoB or rpoC, which encode the β and β′ subunits of RNAP. Phenotypic, structural, and gene expression analyses reveal that suppressor mutants can be divided into two classes; one is specific in its effect on stringent response-regulated genes and shares striking similarity with suppressor mutants of Escherichia coli strains that lack ppGpp, and another reduces transcription of all genes tested in comparison to that in the relA parent strain. Our findings indicate that the ability to successfully establish symbiosis is tightly coupled with the bacteria's ability to undergo global physiological adjustment via the stringent response.
机译:苜蓿中华根瘤菌和苜蓿苜蓿之间的固氮共生需要双方共同进行复杂的生理适应。细菌协调控制生理适应的一种方法是严格应答,该应答是由核苷酸四磷酸鸟苷(ppGpp)的存在触发的。 RelA酶产生的ppGpp被认为与RNA聚合酶(RNAP)结合并改变其启动和延长转录的能力,并影响核心酶对各种sigma因子的亲和力。一个 S。先前已证明不能产生ppGpp的meliloti relA 突变体在形成结节的能力上存在缺陷。该突变体还产生了共生必需的胞外多糖,称为琥珀聚糖(38)。本文介绍的工作涵盖了从宿主植物中分离的抑制子突变体的分析,这些抑制子抑制了 relA 突变体的共生缺陷。所有抑制突变都是外源性的,并映射到 rpoB rpoC ,它们编码RNAP的β和β'亚基。通过表型,结构和基因表达分析,发现抑制突变体可分为两类。一种在对严格的应答调控基因有特效,并且与缺乏ppGpp的大肠杆菌菌株的抑制突变体具有惊人的相似性,另一种与相比降低了所有测试基因的转录> relA 亲本菌株。我们的发现表明,成功建立共生的能力与细菌通过严格反应进行整体生理调节的能力紧密相关。

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