ArticleMicrobiology (Reading, England)2012
Substitutions in the Escherichia coli RNA polymerase inhibitor T7 Gp2 that allow inhibition of transcription when the primary interaction interface between Gp2 and RNA polymerase becomes compromised.
Article in Microbiology (Reading, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Enhanced genetic stability and expression control in growth-decoupled continuous two-stage E. coli fermentations using plasmid-dependent thyA auxotrophic selection.Microbial cell factories · 2025Article
- Phage therapy as a renewed therapeutic approach to mycobacterial infections: a comprehensive review.Infection and drug resistance · 2019Article
- Phenotypic consequences of RNA polymerase dysregulation in Escherichia coli.Nucleic acids research · 2017Article
- Full shut-off of Escherichia coli RNA-polymerase by T7 phage requires a small phage-encoded DNA-binding protein.Nucleic acids research · 2017Article
- Phage T7 Gp2 inhibition of Escherichia coli RNA polymerase involves misappropriation of σ70 domain 1.1.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Transcriptional downregulation of agr expression in Staphylococcus aureus during growth in human serum can be overcome by constitutively active mutant forms of the sensor kinase AgrC.FEMS microbiology letters · 2013Article
- Revenge of the phages: defeating bacterial defences.Nature reviews. Microbiology · 2013Review
- A non-bacterial transcription factor inhibits bacterial transcription by a multipronged mechanism.RNA biology · 2013Article
- Overexpression of Escherichia coli udk mimics the absence of T7 Gp2 function and thereby abrogates successful infection by T7 phage.Microbiology (Reading, England) · 2013Article
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Authors and funding
5 authors at 2 institutions in 3 countries.
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Abstract
The Escherichia coli-infecting bacteriophage T7 encodes a 7 kDa protein, called Gp2, which is a potent inhibitor of the host RNA polymerase (RNAp). Gp2 is essential for T7 phage development. The interaction site for Gp2 on the E. coli RNAp is the β' jaw domain, which is part of the DNA binding channel. The binding of Gp2 to the β' jaw antagonizes several steps associated with interactions between the RNAp and promoter DNA, leading to inhibition of transcription at the open promoter complex formation step. In the structure of the complex formed between Gp2 and a fragment of the β' jaw, amino acid residues in the β3 strand of Gp2 contribute to the primary interaction interface with the β' jaw. The 7009 E. coli strain is resistant to T7 because it carries a charge reversal point mutation in the β' jaw that prevents Gp2 binding. However, a T7 phage encoding a mutant form of Gp2, called Gp2(β), which carries triple amino acid substitutions E24K, F27Y and R56C, can productively infect this strain. By studying the molecular basis of inhibition of RNAp from the 7009 strain by Gp2(β), we provide several lines of evidence that the E24K and F27Y substitutions facilitate an interaction with RNAp when the primary interaction interface with the β' jaw is compromised. The proposed additional interaction interface between RNAp and Gp2 may contribute to the multipronged mechanism of transcription inhibition by Gp2.
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