Enterotoxigenic Escherichia coli (ETEC) is a major cause of traveller’s and infantile diarrhoea in developing countries, and results in considerable mortality in under 5 year olds. Disease is mediated through adhesion of ETEC cells to the intestinal brush border and the secretion of the heat-stable and/or heat-labile toxin. Whilst the toxins have been well studied it is still not clear how their expression is regulated. This work has defined binding of CRP, H-NS and σ\(^7\)\(^0\) across the genome of the prototypical ETEC strain H10407. We demonstrate a central role for all three factors in regulating pathogenicity in ETEC H10407. Hence, we show that CRP directly regulates expression of both \(estA2\) and \(estA1\), which encode the heat-stable toxins. Furthermore, CRP indirectly represses expression of the heat-labile toxin. This work also identifies a role for CRP in controlling transcription of a small open reading frame, imbedded within a gene, at the 3’ end of an operon encoding a type I secretion system.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:636834 |
| Date | January 2015 |
| Creators | Haycocks, James Richard John |
| Publisher | University of Birmingham |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://etheses.bham.ac.uk//id/eprint/5650/ |
Page generated in 0.0016 seconds