ArticleGenetics2006
Roles of PriA protein and double-strand DNA break repair functions in UV-induced restriction alleviation in Escherichia coli.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- ArdB Protective Activity for Unmodified λ Phage Against EcoKI Restriction Decreases in UV-Treated Escherichia coli.Current microbiology · 2019Article
- Mechanisms of bacterial DNA replication restart.Nucleic acids research · 2018Review
- Cellular localization and dynamics of the Mrr type IV restriction endonuclease of Escherichia coli.Nucleic acids research · 2014Article
- Cleavage of a model DNA replication fork by a methyl-specific endonuclease.Nucleic acids research · 2011Article
- Conflicts targeting epigenetic systems and their resolution by cell death: novel concepts for methyl-specific and other restriction systems.DNA research : an international journal for rapid publication of reports on genes and genomes · 2010Review
- Recruitment to stalled replication forks of the PriA DNA helicase and replisome-loading activities is essential for survival.DNA repair · 2010Review
- Cleavage of a model DNA replication fork by a Type I restriction endonuclease.Nucleic acids research · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been widely considered that DNA modification protects the chromosome of bacteria E. coli K-12 against their own restriction-modification systems. Chromosomal DNA is protected from degradation by methylation of target sequences. However, when unmethylated target sequences are generated in the host chromosome, the endonuclease activity of the EcoKI restriction-modification enzyme is inactivated by the ClpXP protease and DNA is protected. This process is known as restriction alleviation (RA) and it can be induced by UV irradiation (UV-induced RA). It has been proposed that chromosomal unmethylated target sequences, a signal for the cell to protect its own DNA, can be generated by homologous recombination during the repair of damaged DNA. In this study, we wanted to further investigate the genetic requirements for recombination proteins involved in the generation of unmethylated target sequences. For this purpose, we monitored the alleviation of EcoKI restriction by measuring the survival of unmodified lambda in UV-irradiated cells. Our genetic analysis showed that UV-induced RA is dependent on the excision repair protein UvrA, the RecA-loading activity of the RecBCD enzyme, and the primosome assembly activity of the PriA helicase and is partially dependent on RecFOR proteins. On the basis of our results, we propose that unmethylated target sequences are generated at the D-loop by the strand exchange of two hemi-methylated duplex DNAs and subsequent initiation of DNA replication.
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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.