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CRP-dependent Positive Autoregulation and Proteolytic Degradation Regulate Competence Activator Sxy of Escherichia coli

Lookup NU author(s): Dr Milena Jaskolska, Professor Kenn Gerdes

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Abstract

© 2014 John Wiley & Sons Ltd. Summary: Natural competence, the ability of bacteria to take up exogenous DNA and incorporate it into their chromosomes, is in most bacteria a transient phenomenon under complex genetic and environmental control. In the Gram-negative bacteria Haemophilus influenzae and Vibrio cholerae, the master regulator Sxy/TfoX controls competence development. Although not known to be naturally competent, Escherichia coli possesses a Sxy homologue and a competence regulon containing the genes required for DNA uptake. Here, we show that in contrast to other characterised Gamma-proteobacteria, E.coliSxy is positively autoregulated at the level of transcription by a mechanism that requires cAMP receptor protein (CRP), cyclic AMP (cAMP) and a CRP-S site in the sxy promoter. Similarly, we found no evidence that Sxy expression in E.coli was regulated at the translational level. However, our analysis revealed that Sxy is an unstable protein and that its cellular level is negatively regulated at the post-translational level via degradation by Lon protease. Interestingly, in the Gram-positive model organism Bacillus subtilis, the competence master regulator ComK is also positively autoregulated at the level of transcription and negatively regulated by proteolysis. Together, these findings reveal striking similarities between the competence regulons of a Gram-positive and a Gram-negative bacterium.


Publication metadata

Author(s): Jaskolska M, Gerdes K

Publication type: Article

Publication status: Published

Journal: Molecular Microbiology

Year: 2015

Volume: 95

Issue: 5

Pages: 833-845

Print publication date: 01/03/2015

Online publication date: 24/01/2015

Acceptance date: 02/12/2014

ISSN (print): 0950-382X

ISSN (electronic): 1365-2958

Publisher: Blackwell Publishing Ltd

URL: http://doi.org/10.1111/mmi.12901

DOI: 10.1111/mmi.12901

PubMed id: 25491382


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