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Protection against deleterious nitrogen compounds: role of sigma(S)-dependent small RNAs encoded adjacent to sdiA

机译:防止有害的氮化合物:与sdiA相邻编码的依赖sigma(S)的小RNA的作用

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摘要

Here, we report the characterization of a set of small, regulatory RNAs (sRNAs) expressed from an Escherichia coli locus we have denoted sdsN located adjacent to the LuxR-homolog gene sdiA. Two longer sRNAs, SdsN(137) and SdsN(178) are transcribed from two sigma(S)-dependent promoters but share the same terminator. Low temperature, rich nitrogen sources and the Crl and NarP transcription factors differentially affect the levels of the SdsN transcripts. Whole genome expression analysis after pulse overexpression of SdsN(137) and assays of lacZ fusions revealed that the SdsN(137) directly represses the synthesis of the nitroreductase NfsA, which catalyzes the reduction of the nitrogroup (NO2) in nitroaromatic compounds and the flavohemoglobin HmpA, which has aerobic nitric oxide (NO) dioxygenase activity. Consistent with this regulation, SdsN(137) confers resistance to nitrofurans. In addition, SdsN(137) negatively regulates synthesis of NarP. Interestingly, SdsN(178) is defective at regulating the above targets due to unusual binding to the Hfq protein, but cleavage leads to a shorter form, SdsN(124), able to repress nfsA and hmpA.
机译:在这里,我们报道了从大肠杆菌基因座表达的一组小调控RNA(sRNA)的表征,我们已将其标记为与LuxR同源基因sdiA相邻的sdsN。两个更长的sRNA,SdsN(137)和SdsN(178)从两个sigma(S)依赖性启动子转录而来,但它们共享相同的终止子。低温,丰富的氮源以及Crl和NarP转录因子差异影响SdsN转录本的水平。 SdsN(137)脉冲过表达后的全基因组表达分析和lacZ融合实验表明,SdsN(137)直接抑制硝基还原酶NfsA的合成,催化硝基芳族化合物和黄血红蛋白HmpA中硝基基团(NO2)的还原。 ,具有需氧一氧化氮(NO)双加氧酶活性。与该法规一致,SdsN(137)具有对硝基呋喃的抗性。此外,SdsN(137)负调节NarP的合成。有趣的是,由于与Hfq蛋白的异常结合,SdsN(178)在调节上述靶标方面存在缺陷,但切割导致形成一个较短的形式SdsN(124),能够抑制nfsA和hmpA。

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