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首页> 外文期刊>Journal of Molecular Biology >Regulation of RNA polymerase promoter selectivity by covalent modification of DNA.
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Regulation of RNA polymerase promoter selectivity by covalent modification of DNA.

机译：通过DNA的共价修饰来调节RNA聚合酶启动子的选择性。

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摘要

Expression of genes encoding type II restriction/modification (R/M) systems, which are widely spread in eubacteria, must be tightly regulated to ensure that host DNA is protected from restriction endonucleases at all times. Examples of coordinated expression of R/M genes that rely on the action of regulatory factors or the ability of methyl transferases to repress their own synthesis by interacting with the promoter DNA have been described. Here, we characterize the molecular mechanism of factor-independent regulation in the CfrBI R/M system. Regulation of the cfrBIM gene transcription occurs through CfrBIM-catalyzed methylation of a cytosine residue in the cfrBIM promoter. The covalent modification inhibits cfrB1M promoter complex formation by interfering with the RNA polymerase sigma(70) subunit region 4.2 recognition of the -35 promoter element. The decrease in the cfrBIM promoter complex formation leads to increase in the activity of overlapping cfrBIR promoters. This elegant factor-independent regulatory system ensures coordinated expression of the cfrBI genes.
机译：编码II型限制/修饰（R / M）系统的基因的表达必须在真细菌中广泛传播，必须对其进行严格调节，以确保始终保护宿主DNA不受限制核酸内切酶的影响。已经描述了依赖于调节因子或甲基转移酶通过与启动子DNA相互作用来抑制其自身合成的能力的R / M基因的协同表达的实例。在这里，我们表征了CfrBI R / M系统中因子独立调节的分子机制。 cfrBIM基因转录的调节是通过cfrBIM启动子中胞嘧啶残基的CfrBIM催化甲基化而发生的。共价修饰通过干扰-35启动子元件的RNA聚合酶sigma（70）亚基区域4.2识别来抑制cfrB1M启动子复合物的形成。 cfrBIM启动子复合物形成的减少导致重叠的cfrBIR启动子的活性增加。这种优雅的因子独立调节系统可确保cfrBI基因的协调表达。

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