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.
journal_name
Proc Natl Acad Sci U S Aauthors
Bhat A,Shin M,Jeong JH,Kim HJ,Lim HJ,Rhee JH,Paik SY,Takeyasu K,Tobe T,Yen H,Lee G,Choy HEdoi
10.1073/pnas.1322033111subject
Has Abstractpub_date
2014-06-24 00:00:00pages
E2586-95issue
25eissn
0027-8424issn
1091-6490pii
1322033111journal_volume
111pub_type
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