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首页> 外文期刊>Journal of Molecular Biology >A multipartite interaction between Salmonella transcription factorsigma(28) and its anti-sigma factor FlgM: Implications for sigma(28)holoenzyme destabilization through stepwise binding
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A multipartite interaction between Salmonella transcription factorsigma(28) and its anti-sigma factor FlgM: Implications for sigma(28)holoenzyme destabilization through stepwise binding

机译：沙门氏菌转录因子sigma（28）及其抗sigma因子FlgM之间的多方相互作用：sigma（28）整体酶通过逐步结合去稳定的含义

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摘要

Transcription of the late (Class 3) flagellar promoters in Salmonella typhimurium is dependent upon the flagellar specific sigma factor, sigma (28), encoded by the fliA gene. sigma (28)-dependent transcription is inhibited by an anti-sigma factor, FlgM, through a direct interaction. FLgM can bind both to free sigma (28) to prevent it from forming a complex with core RNA polymerase, and to sigma (28) holoenzyme to destabilize the complex. A collection of fliA mutants defective for negative regulation by FlgM (fliA* mutants) were isolated. This collection included 27 substitution mutations that conferred insensitivity to FlgM in vivo. The distribution of mutations defined three potential FlgM binding domains in conserved sigma factor regions 2.1, 3.1 and 4 of sigma (28). A subset of mutants from each region was assayed for FlgM binding and transcriptional activity in vitro. The results strongly support a multipartite interaction between sigma (28) and FlgM. Region 4 mutations, but not region 2.1 or 3.1 mutations, interfered with the ability of FIRM to destabilize sigma (28) from core RNA polymerase. We present refined models for FlgM inhibition of sigma (28) and for FlgM destabilization of sigma (28) holoenzyme.
机译：鼠伤寒沙门氏菌中晚期（第3类）鞭毛启动子的转录取决于fliA基因编码的鞭毛特异性sigma因子sigma（28）。 σ（28）依赖性转录通过直接相互作用被抗σ因子FlgM抑制。 FLgM既可以与游离sigma（28）结合以防止其与核心RNA聚合酶形成复合物，也可以与sigma（28）全酶结合以使复合物不稳定。分离了由flgM的负调控缺陷的fliA突变体的集合（fliA *突变体）。该集合包括27个取代突变，这些突变赋予了体内对FlgM的不敏感性。突变的分布在σ的保守σ因子区域2.1、3.1和4中定义了三个潜在的FlgM结合域（28）。在体外测定了来自每个区域的突变体的子集的FlgM结合和转录活性。结果强烈支持sigma（28）和FlgM之间的多方交互。区域4的突变，而不是区域2.1或3.1的突变，干扰了FIRM从核心RNA聚合酶中破坏sigma（28）的能力。我们为Sigma（28）的FlgM抑制和Sigma（28）的全酶FlgM不稳定提供了精确的模型。

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