ArticleNucleic acids research2009
IHF-binding sites inhibit DNA loop formation and transcription initiation.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
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- Structural interplay between DNA-shape protein recognition and supercoiling: The case of IHF.Computational and structural biotechnology journal · 2022Article
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- Engineered CRISPRa enables programmable eukaryote-like gene activation in bacteria.Nature communications · 2019Article
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- Production of DNA minicircles less than 250 base pairs through a novel concentrated DNA circularization assay enabling minicircle design with NF-κB inhibition activity.Nucleic acids research · 2017Article
- CRP-cyclic AMP dependent inhibition of the xylene-responsive σ(54)-promoter Pu in Escherichia coli.PloS one · 2014Article
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- Sequence dependence of DNA bending rigidity.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Transcriptional activation of enhancer and sigma(54)-dependent promoters requires efficient interactions between enhancer-binding proteins (EBP) and promoter bound sigma(54)-RNA polymerase (E sigma(54)) achieved by DNA looping, which is usually facilitated by the integration host factor (IHF). Since the lengths of the intervening region supporting DNA-loop formation are similar among IHF-dependent and IHF-independent promoters, the precise reason(s) why IHF is selectively important for the frequency of transcription initiation remain unclear. Here, using kinetic cyclization and in vitro transcription assays we show that, in the absence of IHF protein, the DNA fragments containing an IHF-binding site have much less looping-formation ability than those that lack an IHF-binding site. Furthermore, when an IHF consensus-binding site was introduced into the intervening region between promoter and enhancer of the target DNA fragments, loop formation and DNA-loop-dependent transcriptional activation are significantly reduced in a position-independent manner. DNA-looping-independent transcriptional activation was unaffected. The binding of IHF to its consensus site in the target promoters clearly restored efficient DNA looping formation and looping-dependent transcriptional activation. Our data provide evidence that one function for the IHF protein is to release a communication block set by intrinsic properties of the IHF DNA-binding site.
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