Abstract
Enteropathogenic E. coli causes attaching and effacing (A/E) intestinal lesions. The genes involved in the formation of A/E lesions are encoded within a chromosomal island comprising of five major operons, LEE1-5. The global regulator H-NS represses the expression of these operons. Ler, a H-NS homologue, counteracts the H-NS–mediated repression. Using a novel genetic approach, we identified the amino acid residues in Ler that are involved in the interaction with H-NS: I20 and L23 in the C-terminal portion of α-helix 3, and I42 in the following unstructured linker region.
Original language | English |
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Pages (from-to) | 559-564 |
Number of pages | 6 |
Journal | Journal of Microbiology |
Volume | 54 |
Issue number | 8 |
DOIs | |
State | Published - 1 Aug 2016 |
Keywords
- enteropathogenic E. coli (EPEC)
- H-NS
- LEE
- Ler
- transcription repression