ArticleMolecular microbiology2014
Stringent response processes suppress DNA damage sensitivity caused by deficiency in full-length translation initiation factor 2 or PriA helicase.
Article in Molecular microbiology, 2014. 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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Who cites it
12 citing papers in PubMed.
- Dysregulated DnaB unwinding induces replisome decoupling and daughter strand gaps that are countered by RecA polymerization.Nucleic acids research · 2024Article
- Control of transcription elongation and DNA repair by alarmone ppGpp.Nature structural & molecular biology · 2023Article
- Modulation of RecFORQ- and RecA-Mediated Homologous Recombination in Escherichia coli by Isoforms of Translation Initiation Factor IF2.Journal of bacteriology · 2022Article
- Essential Role for an Isoform of Escherichia coli Translation Initiation Factor IF2 in Repair of Two-Ended DNA Double-Strand Breaks.Journal of bacteriology · 2022Article
- How the initiating ribosome copes with ppGpp to translate mRNAs.PLoS biology · 2020Article
- DksA-RNA polymerase interactions support new origin formation and DNA repair in Escherichia coli.Molecular microbiology · 2019Article
- Genes within Genes in Bacterial Genomes.Microbiology spectrum · 2018Review
- Decreased Expression of Stable RNA Can Alleviate the Lethality Associated with RNase E Deficiency in Escherichia coli.Journal of bacteriology · 2017Article
- From Mfd to TRCF and Back Again-A Perspective on Bacterial Transcription-coupled Nucleotide Excision Repair.Photochemistry and photobiology · 2017Review
- ppGpp couples transcription to DNA repair in E. coli.Science (New York, N.Y.) · 2016Article
- Diversity in (p)ppGpp metabolism and effectors.Current opinion in microbiology · 2015Review
- Genome sequence and phenotypic characterization of Caulobacter segnis.Current microbiology · 2015Article
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6 authors.
Funding
Abstract
When Escherichia coli grows in the presence of DNA-damaging agents such as methyl methanesulphonate (MMS), absence of the full-length form of Translation Initiation Factor 2 (IF2-1) or deficiency in helicase activity of replication restart protein PriA leads to a considerable loss of viability. MMS sensitivity of these mutants was contingent on the stringent response alarmone (p)ppGpp being at low levels. While zero levels (ppGpp°) greatly aggravated sensitivity, high levels promoted resistance. Moreover, M+ mutations, which suppress amino acid auxotrophy of ppGpp° strains and which have been found to map to RNA polymerase subunits, largely restored resistance to IF2-1- and PriA helicase-deficient mutants. The truncated forms IF2-2/3 played a key part in inducing especially severe negative effects in ppGpp° cells when restart function priB was knocked out, causing loss of viability and severe cell filamentation, indicative of SOS induction. Even a strain with the wild-type infB allele exhibited significant filamentation and MMS sensitivity in this background whereas mutations that prevent expression of IF2-2/3 essentially eliminated filamentation and largely restored MMS resistance. The results suggest different influences of IF2-1 and IF2-2/3 on the replication restart system depending on (p)ppGpp levels, each having the capacity to maximize survival under differing growth conditions.
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