首页> 美国卫生研究院文献>Journal of Bacteriology >Intersubunit Complementation of Sugar Signal Transduction in VirA Heterodimers and Posttranslational Regulation of VirA Activity in Agrobacterium tumefaciens
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Intersubunit Complementation of Sugar Signal Transduction in VirA Heterodimers and Posttranslational Regulation of VirA Activity in Agrobacterium tumefaciens

机译:VirA异二聚体中糖信号传导的亚基间互补和根癌农杆菌中VirA活性的翻译后调控。

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摘要

The VirA/VirG two-component regulatory system of Agrobacterium tumefaciens regulates expression of the virulence (vir) genes that control the infection process leading to crown gall tumor disease on susceptible plants. VirA, a membrane-bound homodimer, initiates vir gene induction by communicating the presence of molecular signals found at the site of a plant wound through phosphorylation of VirG. Inducing signals include phenols, monosaccharides, and acidic pH. While sugars are not essential for gene induction, their presence greatly increases vir gene expression when levels of the essential phenolic signal are low. Reception of the sugar signal depends on a direct interaction between ChvE, a sugar-binding protein, and VirA. Here we show that the sugar signal received in the periplasmic region of one subunit within a VirA heterodimer can enhance the kinase function of the second subunit. However, sugar enhancement of vir gene expression was vector dependent. virA alleles expressed from pSa-derived vectors inhibited signal transduction by endogenous VirA. Inhibition was conditional, depending on the induction medium and the virA allele tested. Moreover, constitutive expression of virG overcame the inhibitory effect of some but not all virA alleles, suggesting that there may be more than one inhibitory mechanism.
机译:根癌土壤杆菌的VirA / VirG两组分调节系统调节可控制植物上导致冠gall瘤病的感染过程的毒力(vir)基因的表达。 VirA是一种与膜结合的同型二聚体,通过传达通过VirG的磷酸化作用在植物伤口部位发现的分子信号的存在来启动vir基因的诱导。诱导信号包括苯酚,单糖和酸性pH。尽管糖不是基因诱导所必需的,但当必需酚信号的水平较低时,糖的存在会大大提高vir基因的表达。糖信号的接收取决于糖结合蛋白ChvE和VirA之间的直接相互作用。在这里,我们显示在VirA异二聚体中一个亚基的周质区域中接收到的糖信号可以增强第二个亚基的激酶功能。但是,vir基因表达的糖增强是载体依赖性的。从pSa衍生的载体表达的virA等位基因抑制了内源性VirA的信号转导。抑制是有条件的,具体取决于诱导培养基和测试的virA等位基因。此外,virG的组成型表达克服了某些但不是全部virA等位基因的抑制作用,表明可能存在不止一种抑制机制。

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