1887

Abstract

Expression of the operon is subject to catabolite repression by glucose. It was shown that a -acting catabolite-responsive element (CRE) sequence located 64 bp downstream of the transcription-start site mediated catabolite repression of the operon as it does for many other genes. Point mutations in the CRE sequence caused the loss of catabolite repression of the operon. Catabolite repression of expression was relieved in a 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 expression. By the use of gel mobility shift analysis, a specific HPr-P dependent binding of CcpA to the CRE site was demonstrated.

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2000-11-01
2020-04-04
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