Abstract
Transcription of the LEE] 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 PIA, which can drive transcript initiation 10 bp upstream of the PI promoter transcript start point. Because of the overlap between P1 and PIA, PIA 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 PIA 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 PIA promoter. We propose that such promoter elements may play a role in enforcing specificity in bacterial regulatory regions that contain alternative possible promoters.
Original language | English |
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Pages (from-to) | 681-686 |
Number of pages | 6 |
Journal | Biochemical Journal |
Volume | 436 |
DOIs | |
Publication status | Published - 1 Jun 2011 |
Keywords
- transcription initiation
- promoter discrimination
- mutational analysis
- bacterial promoter
- bacterial multi-subunit RNA polymerase