ArticleJournal of bacteriology2004
Protective role for H-NS protein in IS1 transposition.
Article in Journal of bacteriology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Active Transposition of Insertion Sequences in Prokaryotes: Insights from the Response ofAntioxidants (Basel, Switzerland) · 2022Review
- Tetracycline Antibiotics and Resistance.Cold Spring Harbor perspectives in medicine · 2016Review
- The genetic basis of Escherichia coli pathoadaptation to macrophages.PLoS pathogens · 2013Article
- Transcription of AAT•ATT triplet repeats in Escherichia coli is silenced by H-NS and IS1E transposition.PloS one · 2010Article
- H-NS binds with high affinity to the Tn10 transpososome and promotes transpososome stabilization.Nucleic acids research · 2009Article
- The global bacterial regulator H-NS promotes transpososome formation and transposition in the Tn5 system.Nucleic acids research · 2009Article
- Increased genome instability in Escherichia coli lon mutants: relation to emergence of multiple-antibiotic-resistant (Mar) mutants caused by insertion sequence elements and large tandem genomic amplifications.Antimicrobial agents and chemotherapy · 2007Article
- The global regulator H-NS acts directly on the transpososome to promote Tn10 transposition.Genes & development · 2005Article
- Genomes are covered with ubiquitous 11 bp periodic patterns, the "class A flexible patterns".BMC bioinformatics · 2005Article
- Genetic evidence that GTP is required for transposition of IS903 and Tn552 in Escherichia coli.Journal of bacteriology · 2005Article
- Metabolic engineering in the -omics era: elucidating and modulating regulatory networks.Microbiology and molecular biology reviews : MMBR · 2005Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transposase (InsAB') of the insertion element IS1 can create breaks in DNA that lead to induction of the SOS response. We have used the SOS response to InsAB' to screen for host mutations that affect InsAB' function and thus point to host functions that contribute to the IS1 transposition mechanism. Mutations in the hns gene, which codes for a DNA binding protein with wide-ranging effects on gene expression, abolish the InsAB'-induced SOS response. They also reduce transposition, whether by simple insertion or cointegrate formation, at least 100-fold compared with the frequency seen in hns+ cells. Examination of protein profiles revealed that in an hns-null mutant, InsAB' is undetectable under conditions where it constitutes the most abundant protein in hns+ cells. Likewise, brief labeling of the hns cells with [35S]methionine revealed very small amounts of InsAB', and this was undetectable after a short chase. Transcription from the promoters used to express insAB' was essentially unaltered in hns cells, as was the level of insAB' mRNA. A mutation in lon, but not in ftsH or clpP, restored InsAB' synthesis in the hns strain, and a mutation in ssrA partially restored it, implying that the absence of H-NS leads to a problem in completing translation of insAB' mRNA and/or degradation of nascent InsAB' protein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.