ArticleJournal of bacteriology2009
UvrD303, a hyperhelicase mutant that antagonizes RecA-dependent SOS expression by a mechanism that depends on its C terminus.
Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- UvrD helicase-RNA polymerase interactions are governed by UvrD's carboxy-terminal Tudor domain.Communications biology · 2020Article
- Free-energy simulations reveal molecular mechanism for functional switch of a DNA helicase.eLife · 2018Article
- Rad51 Nucleoprotein Filament Disassembly Captured Using Fluorescent Plasmodium falciparum SSB as a Reporter for Single-Stranded DNA.PloS one · 2016Article
- Article
- Suppression of the E. coli SOS response by dNTP pool changes.Nucleic acids research · 2015Article
- Active displacement of RecA filaments by UvrD translocase activity.Nucleic acids research · 2015Article
- Escherichia coli radD (yejH) gene: a novel function involved in radiation resistance and double-strand break repair.Molecular microbiology · 2015Article
- The UvrD303 hyper-helicase exhibits increased processivity.The Journal of biological chemistry · 2014Article
- Article
- The conserved C-terminus of the PcrA/UvrD helicase interacts directly with RNA polymerase.PloS one · 2013Article
- Modulation of UvrD helicase activity by covalent DNA-protein cross-links.The Journal of biological chemistry · 2010Article
- Lessons learned from UvrD helicase: mechanism for directional movement.Annual review of biophysics · 2010Review
- An N-terminal clamp restrains the motor domains of the bacterial transcription-repair coupling factor Mfd.Nucleic acids research · 2009Article
- Suppression of constitutive SOS expression by recA4162 (I298V) and recA4164 (L126V) requires UvrD and RecX in Escherichia coli K-12.Molecular microbiology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genomic integrity is critical for an organism's survival and ability to reproduce. In Escherichia coli, the UvrD helicase has roles in nucleotide excision repair and methyl-directed mismatch repair and can limit reactions by RecA under certain circumstances. UvrD303 (D403A D404A) is a hyperhelicase mutant, and when expressed from a multicopy plasmid, it results in UV sensitivity (UV(s)), recombination deficiency, and antimutability. In order to understand the molecular mechanism underlying the UV(s) phenotype of uvrD303 cells, this mutation was transferred to the E. coli chromosome and studied in single copy. It is shown here that uvrD303 mutants are UV sensitive, recombination deficient, and antimutable and additionally have a moderate defect in inducing the SOS response after UV treatment. The UV-sensitive phenotype is epistatic with recA and additive with uvrA and is partially suppressed by removing the LexA repressor. Furthermore, uvrD303 is able to inhibit constitutive SOS expression caused by the recA730 mutation. The ability of UvrD303 to antagonize SOS expression was dependent on its 40 C-terminal amino acids. It is proposed that UvrD303, via its C terminus, can decrease the levels of RecA activity in the cell.
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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.