期刊
JOURNAL OF BACTERIOLOGY
卷 193, 期 7, 页码 1622-1632出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.01082-10
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资金
- John Sealy Memorial Endowment Fund
- NIH [AI079154-01A2]
- VIEP-BUAP [MALI-NAT09-I]
- Consejo Nacional de Ciencia y Tecnologia (CONACyT) [60796]
- Direccion General de Asuntos del Personal Academico [IN227410]
- CONACYT, Mexico
- SURP, UTMB
- ARRA NIH [AI079154-01A2S1]
Long polar fimbriae 1 (Lpf1) of Escherichia coli O157:H7 is a tightly regulated adhesin, with H-NS silencing the transcriptional expression of the lpf1 operon while Ler (locus of enterocyte effacement-encoded regulator) acts as an antisilencer. We mapped the minimal regulatory region of lpf1 required for H-NS- and Ler-mediated regulation and found that it is 79% AT rich. Three putative sites for H-NS binding were identified. Two of them, named silencer regulatory sequence 1 (SRS1) and SRS2, are located on a region that covers both of the lpf1 promoters (P1 and P2). The third putative H-NS binding site is located within the lpfA1 gene in a region extending from +258 bp to +545 bp downstream of ATG; however, this site does not seem to play a role in lpfA1 regulation under the conditions tested in this work. Ler was also found to interact with Ler binding sites (LBSs). Ler binding site 1 (LBS1) and LBS2 are located upstream of the two promoters. LBS1 overlaps SRS1, while LBS3 overlaps the P1 promoter and SRS2. Based on the experimental data, we propose that H-NS silences lpf1 expression by binding to both of the SRSs on the promoter region, forming an SRS-H-NS complex that prevents RNA polymerase-mediated transcription. A model of the regulation of the lpfA1 operon of E. coli O157:H7 by H-NS and Ler is discussed.
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