Evidence map›Paper›PMID 10217781›Full record

ArticleJournal of bacteriology1999

DNA polymerase II (polB) is involved in a new DNA repair pathway for DNA interstrand cross-links in Escherichia coli.

M Berardini, P L Foster, E L Loechler

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

57 citing papers in PubMed, 116 citations in OpenAlex.

  1. Combining Electrochemical Reduction with Biosynthesis for Directed Conversion of COAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  4. Discovery, implications and initial use of semi-synthetic organisms with an expanded genetic alphabet/code.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Chloroethylating anticancer drug-induced mutagenesis and its repair inGenes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019
    Article
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  11. Article
  12. Review
  13. Article
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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

3 authors at 1 institution in 1 country.

M BerardiniDepartment of Biology, Boston University, Boston, Massachusetts 02215, USA.
P L Foster
E L Loechler
Boston University · US

Funding

INTERSTRAND CROSSLINKS--REPLICATION, REPAIR, MUTATIONSR01CA049198 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LOECHLER, EDWARD L · 1993 to 1995
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CYCLOPHOSPHAMIDE &IFOSFAMIDE--PREFERRED DNA CROSSLINKSR01CA063396 · NCI · SOUTHERN RESEARCH INSTITUTE · PI STRUCK, ROBERT F · 1994 to 1996
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INTERACTIONS AMONG REPLICATION AND MUTATION PROTEINSR01GM054084 · NIGMS · INDIANA UNIVERSITY BLOOMINGTON · PI FOSTER, PATRICIA L. · 1997 to 1999
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NCI NIH HHS CA49198NCI NIH HHS CA63396NIGMS NIH HHS R01 GM054084
6 · The paper itself

Abstract

DNA-DNA interstrand cross-links are the cytotoxic lesions for many chemotherapeutic agents. A plasmid with a single nitrogen mustard (HN2) interstrand cross-link (inter-HN2-pTZSV28) was constructed and transformed into Escherichia coli, and its replication efficiency (RE = [number of transformants from inter-HN2-pTZSV28]/[number of transformants from control]) was determined to be approximately 0.6. Previous work showed that RE was high because the cross-link was repaired by a pathway involving nucleotide excision repair (NER) but not recombination. (In fact, recombination was precluded because the cells do not receive lesion-free homologous DNA.) Herein, DNA polymerase II is shown to be in this new pathway, since the replication efficiency (RE) is higher in a polB+ ( approximately 0. 6) than in a DeltapolB (approximately 0.1) strain. Complementation with a polB+-containing plasmid restores RE to wild-type levels, which corroborates this conclusion. In separate experiments, E. coli was treated with HN2, and the relative sensitivity to killing was found to be as follows: wild type < polB < recA < polB recA approximately uvrA. Because cells deficient in either recombination (recA) or DNA polymerase II (polB) are hypersensitive to nitrogen mustard killing, E. coli appears to have two pathways for cross-link repair: an NER/recombination pathway (which is possible when the cross-links are formed in cells where recombination can occur because there are multiple copies of the genome) and an NER/DNA polymerase II pathway. Furthermore, these results show that some cross-links are uniquely repaired by each pathway. This represents one of the first clearly defined pathway in which DNA polymerase II plays a role in E. coli. It remains to be determined why this new pathway prefers DNA polymerase II and why there are two pathways to repair cross-links.

Indexed as

DNA RepairDNA Polymerase IIEscherichia coliGenetic Complementation TestMechlorethamineMicrobial Sensitivity TestsMutagensPlasmidsDNA Polymerase IIMechlorethamineMutagens

Identifiers

PMID10217781
PMCPMC93732
OpenAlexW2162699077

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.