DNA looping-dependent autorepression of LEE1 P1 promoters by Ler in enteropathogenic Escherichia coli (EPEC).
Proc Natl Acad Sci U S A
; 111(25): E2586-95, 2014 Jun 24.
Article
em En
| MEDLINE
| ID: mdl-24920590
ABSTRACT
Ler, a homolog of H-NS in enteropathogenic Escherichia coli (EPEC), plays a critical role in the expression of virulence genes encoded by the pathogenic island, locus of enterocyte effacement (LEE). Although Ler acts as an antisilencer of multiple LEE operons by alleviating H-NS-mediated silencing, it represses its own expression from two LEE1 P1 promoters, P1A and P1B, that are separated by 10 bp. Various in vitro biochemical methods were used in this study to elucidate the mechanism underlying transcription repression by Ler. Ler acts through two AATT motifs, centered at position -111.5 on the coding strand and at +65.5 on the noncoding strand, by simultaneously repressing P1A and P1B through DNA-looping. DNA-looping was visualized using atomic force microscopy. It is intriguing that an antisilencing protein represses transcription, not by steric exclusion of RNA polymerase, but by DNA-looping. We propose that the DNA-looping prevents further processing of open promoter complex (RPO) at these promoters during transcription initiation.
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MEDLINE
Assunto principal:
DNA Bacteriano
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Transativadores
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Elementos de Resposta
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Proteínas de Escherichia coli
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Escherichia coli Enteropatogênica
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Loci Gênicos
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Iniciação da Transcrição Genética
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article