Evidence map›Paper›PMID 15489426›Full record

ArticleJournal of bacteriology2004

Isolation of SOS constitutive mutants of Escherichia coli.

Erin K O'Reilly, Kenneth N Kreuzer

Abstract read
In one paragraph

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 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Synthetic lethal mutants inJournal of bacteriology · 2023
    Pooled it
  2. Article
  3. DnaE uses strand displacement synthesis during Okazaki fragment repair.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Completion of DNA replication in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. DNA Methylation.EcoSal Plus · 2014
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Erin K O'ReillyDepartment of Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.
Kenneth N Kreuzer
Duke Medical Center · US

Funding

ANTITUMOR AGENTS AND THE BACTERIOPHAGE T4 TOPOISOMERASER01CA060836 · NCI · DUKE UNIVERSITY · PI KREUZER, KENNETH N · 1993 to 2001
$505k
Direct analysis of fork blockage and DNA repair in vivoR21GM065206 · NIGMS · DUKE UNIVERSITY · PI KREUZER, KENNETH N · 2002 to 2003
$231k
NCI NIH HHS CA 60836NIGMS NIH HHS GM 065206NIGMS NIH HHS R21 GM065206
6 · The paper itself

Abstract

The bacterial SOS regulon is strongly induced in response to DNA damage from exogenous agents such as UV radiation and nalidixic acid. However, certain mutants with defects in DNA replication, recombination, or repair exhibit a partially constitutive SOS response. These mutants presumably suffer frequent replication fork failure, or perhaps they have difficulty rescuing forks that failed due to endogenous sources of DNA damage. In an effort to understand more clearly the endogenous sources of DNA damage and the nature of replication fork failure and rescue, we undertook a systematic screen for Escherichia coli mutants that constitutively express the SOS regulon. We identified mutant strains with transposon insertions in 42 genes that caused increased expression from a dinD1::lacZ reporter construct. Most of these also displayed significant increases in basal levels of RecA protein, confirming an effect on the SOS system. As expected, this collection includes genes, such as lexA, dam, rep, xerCD, recG, and polA, which have previously been shown to cause an SOS constitutive phenotype when inactivated. The collection also includes 28 genes or open reading frames that were not previously identified as SOS constitutive, including dcd, ftsE, ftsX, purF, tdcE, and tynA. Further study of these SOS constitutive mutants should be useful in understanding the multiple causes of endogenous DNA damage. This study also provides a quantitative comparison of the extent of SOS expression caused by inactivation of many different genes in a common genetic background.

Indexed as

MutationDNA, BacterialDNA DamageDNA RepairDNA ReplicationDNA Transposable ElementsEscherichia coliEscherichia coli ProteinsMutagenesis, InsertionalRec A RecombinasesSOS Response, GeneticsDNA, BacterialDNA Transposable ElementsEscherichia coli ProteinsRec A Recombinases

Identifiers

PMID15489426
PMCPMC523190
OpenAlexW2125947686

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.