ArticleProceedings of the National Academy of Sciences of the United States of America2014
DNA looping-dependent autorepression of LEE1 P1 promoters by Ler in enteropathogenic Escherichia coli (EPEC).
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Structural basis of the oligomerization of anti-silencer Ler from enterohemorrhagicStructural dynamics (Melville, N.Y.) · 2026Article
- Post-translational modifications of the nucleoid protein H-NS: sites, mechanisms, and regulatory cues.FEMS microbiology reviews · 2025Review
- The curli regulator CsgD mediates stationary phase counter-silencing of csgBA in Salmonella Typhimurium.Molecular microbiology · 2018Article
- Environment Controls LEE Regulation in EnteropathogenicFrontiers in microbiology · 2018Review
- Amino acid residues in the Ler protein critical for derepression of the LEE5 promoter in enteropathogenic E. coli.Journal of microbiology (Seoul, Korea) · 2016Article
- Article
- Type Three Secretion System in Attaching and Effacing Pathogens.Frontiers in cellular and infection microbiology · 2016Review
- High variation acrossGut microbesArticle
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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