在肠致病性大肠杆菌中，Ler蛋白里对LEE5启动子去阻遏至关重要的氨基酸残基。
Amino acid residues in the Ler protein critical for derepression of the LEE5 promoter in enteropathogenic E. coli.
作者信息
Choi Su-Mi, Jeong Jae-Ho, Choy Hyon E, Shin Minsang
机构信息
Department of Microbiology, Chonnam National University Medical School, Gwangju, 61186, Republic of Korea.
Department of Microbiology, Kyungpook National University School of Medicine, Daegu, 41944, Republic of Korea.
出版信息
J Microbiol. 2016 Aug;54(8):559-64. doi: 10.1007/s12275-016-6027-6. Epub 2016 Aug 2.
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.
肠致病性大肠杆菌会导致肠道出现黏附和抹除（A/E）性病变。参与A/E性病变形成的基因编码于一个包含五个主要操纵子（LEE1 - 5）的染色体岛内。全局调节因子H-NS会抑制这些操纵子的表达。Ler是一种与H-NS同源的蛋白，可抵消H-NS介导的抑制作用。我们采用一种新的遗传学方法，确定了Ler中与H-NS相互作用的氨基酸残基：α螺旋3 C端部分的I20和L23，以及随后的无结构连接区域中的I42。
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