ArticleJournal of bacteriology2000
lon incompatibility associated with mutations causing SOS induction: null uvrD alleles induce an SOS response in Escherichia coli.
Article in Journal of bacteriology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Proteomic survey of the DNA damage response inJournal of bacteriology · 2023Article
- Proteomic survey of the DNA damage response inbioRxiv : the preprint server for biology · 2023Article
- Article
- A new role for Escherichia coli Dam DNA methylase in prevention of aberrant chromosomal replication.Nucleic acids research · 2019Article
- Inactivation of Cell Division Protein FtsZ by SulA Makes Lon Indispensable for the Viability of a ppGpp0 Strain of Escherichia coli.Journal of bacteriology · 2015Article
- Tolerance of Escherichia coli to fluoroquinolone antibiotics depends on specific components of the SOS response pathway.Genetics · 2013Article
- Article
- Pathways of resistance to thymineless death in Escherichia coli and the function of UvrD.Genetics · 2011Article
- UvrD303, a hyperhelicase mutant that antagonizes RecA-dependent SOS expression by a mechanism that depends on its C terminus.Journal of bacteriology · 2009Article
- UvrD controls the access of recombination proteins to blocked replication forks.The EMBO journal · 2007Article
- Characterization of the helicase activity and substrate specificity of Mycobacterium tuberculosis UvrD.Journal of bacteriology · 2007Article
- Genetic evidence for the requirement of RecA loading activity in SOS induction after UV irradiation in Escherichia coli.Journal of bacteriology · 2006Article
- Role for tandem duplication and lon protease in AcrAB-TolC- dependent multiple antibiotic resistance (Mar) in an Escherichia coli mutant without mutations in marRAB or acrRAB.Journal of bacteriology · 2006Article
- Analysis of global gene expression and double-strand-break formation in DNA adenine methyltransferase- and mismatch repair-deficient Escherichia coli.Journal of bacteriology · 2005Article
- Isolation of SOS constitutive mutants of Escherichia coli.Journal of bacteriology · 2004Article
- The Escherichia coli dnaN159 mutant displays altered DNA polymerase usage and chronic SOS induction.Journal of bacteriology · 2004Article
- Evidence for an arginine exporter encoded by yggA (argO) that is regulated by the LysR-type transcriptional regulator ArgP in Escherichia coli.Journal of bacteriology · 2004Article
- The protease Lon and the RNA-binding protein Hfq reduce silencing of the Escherichia coli bgl operon by H-NS.Journal of bacteriology · 2004Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The uvrD gene in Escherichia coli encodes a 720-amino-acid 3'-5' DNA helicase which, although nonessential for viability, is required for methyl-directed mismatch repair and nucleotide excision repair and furthermore is believed to participate in recombination and DNA replication. We have shown in this study that null mutations in uvrD are incompatible with lon, the incompatibility being a consequence of the chronic induction of SOS in uvrD strains and the resultant accumulation of the cell septation inhibitor SulA (which is a normal target for degradation by Lon protease). uvrD-lon incompatibility was suppressed by sulA, lexA3(Ind(-)), or recA (Def) mutations. Other mutations, such as priA, dam, polA, and dnaQ (mutD) mutations, which lead to persistent SOS induction, were also lon incompatible. SOS induction was not observed in uvrC and mutH (or mutS) mutants defective, respectively, in excision repair and mismatch repair. Nor was uvrD-mediated SOS induction abolished by mutations in genes that affect mismatch repair (mutH), excision repair (uvrC), or recombination (recB and recF). These data suggest that SOS induction in uvrD mutants is not a consequence of defects in these three pathways. We propose that the UvrD helicase participates in DNA replication to unwind secondary structures on the lagging strand immediately behind the progressing replication fork, and that it is the absence of this function which contributes to SOS induction in uvrD strains.
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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.