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Catabolite repression of dra–nupC–pdp operon expression in Bacillus subtilis

机译:枯草芽孢杆菌的DRA-NUPC-PDP操纵子表达的分解粘土抑制

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Expression of the Bacillus subtilisdra–nupC–pdp operon is subject to catabolite repression by glucose. It was shown that a cis-acting catabolite-responsive element (CRE) sequence located 64?bp downstream of the transcription-start site mediated catabolite repression of the dra–nupC–pdp operon as it does for many other B. subtilis genes. Point mutations in the CRE sequence caused the loss of catabolite repression of the operon. Catabolite repression of dra–nupC–pdp expression was relieved in a ccpA mutant and was found to be dependent on both HPr and the HPr-like protein Crh. Furthermore, a transcription-repair coupling factor, Mfd, was also found to be involved in the glucose repression of dra–nupC–pdp expression. By the use of in vitro gel mobility shift analysis, a specific HPr-P dependent binding of CcpA to the dra CRE site was demonstrated.
机译:枯草芽孢杆菌的表达对葡萄糖的抑制性抑制。结果表明,位于转录开始部位下游的64°BP的顺式代购响应元件(CRE)序列介导的DRA-NUPC-PDP操纵子的分解代谢物抑制,因为它对枯草芽孢杆菌基因进行了许多。 CRE序列中的点突变导致摩尔枪的抗粘液抑制损失。在CCPA突变体中释放了DRA-NUPC-PDP表达的分解粘土抑制,发现依赖于HPR和HPR样蛋白CRH。此外,还发现转录修复偶联因子MFD,参与DRA-NUPC-PDP表达的葡萄糖抑制。通过使用体外凝胶迁移率移位分析,证实了CCPA对DRA CRE部位的特异性HPR-P依赖性结合。

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