Affiliation:
1. School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, U.K.
Abstract
Transcription of the LEE1 operon in the locus of enterocyte effacement of enterohaemorrhagic Escherichia coli is due to the P1 promoter. Mutational and biochemical analyses reveal the existence of an overlapping promoter, designated P1A, which can drive transcript initiation 10 bp upstream of the P1 promoter transcript start point. Because of the overlap between P1 and P1A, P1A activity is unmasked only when the P1 promoter is inactivated by mutation. In the present paper, we report that mutation of the P1–10 element is less effective in unmasking P1A promoter activity than mutation of the P1–35 element. This suggests that the P1 promoter −35 element, which corresponds to the consensus, can sequester RNA polymerase even when P1 is inactive and thereby prevent RNA polymerase from serving the P1A promoter. We propose that such promoter elements may play a role in enforcing specificity in bacterial regulatory regions that contain alternative possible promoters.
Subject
Cell Biology,Molecular Biology,Biochemistry
Cited by
4 articles.
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