| Title | Amino acid residues in the Ler protein critical for derepression of the LEE5 promoter in enteropathogenic E. coli |
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| Author | Su-Mi Choi1, Jae-Ho Jeong1, Hyon E. Choy1*, and Minsang Shin2* |
| Address | 1Department of Microbiology, Chonnam National University Medical School, Gwangju 61186, Republic of Korea, 2Department of Microbiology, Kyungpook National University School of Medicine, Daegu 41944, Republic of Korea |
| Bibliography | Journal of Microbiology, 54(8),559-564, 2016, |
| DOI | 10.1007/s12275-016-6027-6 |
| Key Words | enteropathogenic E. coli (EPEC), H-NS, LEE, Ler, transcription repression |
| 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. |