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Studies on gene expression in a pathogenic bacterium

Islam , Shahidul MD (2011)
Ph.D. thesis, University of Birmingham.

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Abstract

The activity of the major pathogenicity determinant of enterohaemorrhagic Escherichia coli is primarily coordinated by expression of the LEE1 operon which is part of the locus of enterocyte effacement (LEE). The LEE1 operon regulatory region has been dissected. LEE-encoded transcription factor, GrlA, activates the LEE1 P1 promoter by binding to a target located within the 18 base pair spacer between the promoter 10 and 35 elements. Shortening this spacer to 17 base pairs increases P1 promoter activity and short-circuits GrlA dependent activation, suggesting that GrlA functions like MerR family transcription activators. It was also found that the LEE1 P1 promoter is overlapped by a cryptic promoter, designated P1A. A single base substitution in the P1 consensus -35 element unmasks P1A promoter activity. In contrast, P1A activity is much less when P1 is inactivated by a mutation in its -10 hexamer element. Hence, even when P1 is inactive, the consensus -35 element sequesters RNA polymerase and prevents its access to the P1A promoter. The LEE1 leader sequence also contains a mini-gene that encodes a dipeptide. Genetic studies showed that expression of this mini-gene is important for optimal expression of downstream genes.

Type of Work:Ph.D. thesis.
Supervisor(s):Busby, Steve
School/Faculty:Colleges (2008 onwards) > College of Life & Environmental Sciences
Department:School of Biosciences
Subjects:QR Microbiology
Institution:University of Birmingham
ID Code:1729
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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