Evidence map›Paper›PMID 7665478›Full record

ArticleJournal of bacteriology1995

Suppression of Escherichia coli alkB mutants by Saccharomyces cerevisiae genes.

Y F Wei, B J Chen, L Samson

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Alleviation of 1,N6-ethanoadenine genotoxicity by the Escherichia coli adaptive response protein AlkB.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Linkage map of Escherichia coli K-12, edition 10: the traditional map.Microbiology and molecular biology reviews : MMBR · 1998
    Review
  14. A family of genes required for maintenance of cell wall integrity and for the stress response in Saccharomyces cerevisiae.Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  15. 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

3 authors at 1 institution in 1 country.

Y F WeiDepartment of Molecular and Cellular Toxicology, Harvard School of Public Health, Boston, Massachusetts, USA.
B J Chen
L Samson
Harvard University · US

Funding

EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
STUDIES OF DNA REPAIR USING RHIZOBIUM MELILOTIP01ES003926 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEMPLE, BRUCE F. · 1985 to 1997
–
NCI NIH HHS CA55042NIEHS NIH HHS P01-ESO3926
6 · The paper itself

Abstract

The alkB gene is one of a group of alkylation-inducible genes in Escherichia coli, and its product protects cells from SN2-type alkylating agents such as methyl methanesulfonate (MMS). However, the precise biochemical function of the AlkB protein remains unknown. Here, we describe the cloning, sequencing, and characterization of three Saccharomyces cerevisiae genes (YFW1, YFW12, and YFW16) that functionally complement E. coli alkB mutant cells. DNA sequence analysis showed that none of the three gene products have any amino acid sequence homology with the AlkB protein. The YFW1 and YFW12 proteins are highly serine and threonine rich, and YFW1 contains a stretch of 28 hydrophobic residues, indicating that it may be a membrane protein. The YFW16 gene turned out to be allelic with the S. cerevisiae STE11 gene. STE11 is a protein kinase known to be involved in pheromone signal transduction in S. cerevisiae; however, the kinase activity is not required for MMS resistance because mutant STE11 proteins lacking kinase activity could still complement E. coli alkB mutants. Despite the fact that YFW1, YFW12, and YFW16/STE11 each confer substantial MMS resistance upon E. coli alkB cells, S. cerevisiae null mutants for each gene were not MMS sensitive. Whether these three genes provide alkylation resistance in E. coli via an alkB-like mechanism remains to be determined, but protection appears to be specific for AlkB-deficient E. coli because none of the genes protect other alkylation-sensitive E. coli strains from killing by MMS.

Indexed as

Escherichia coli ProteinsSaccharomyces cerevisiae ProteinsSchizosaccharomyces pombe ProteinsSuppression, GeneticTranscription FactorsAlkylationAmino Acid SequenceBacterial ProteinsBase SequenceCloning, MolecularCytochrome P-450 CYP4ACytochrome P-450 Enzyme SystemDNA, ComplementaryDNA DamageDNA Mutational AnalysisDose-Response Relationship, DrugAlkB protein, E coliBacterial ProteinsCytochrome P-450 CYP4ACytochrome P-450 Enzyme SystemDNA, ComplementaryEscherichia coli ProteinsFungal ProteinsMAP Kinase Kinase KinasesMembrane ProteinsMethyl MethanesulfonateMixed Function OxygenasesPRY2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSchizosaccharomyces pombe ProteinsSte11 protein, S cerevisiaeste11 protein, S pombeTranscription FactorsWSC4 protein, S cerevisiae

Identifiers

PMID7665478
PMCPMC177278
OpenAlexW1489512833

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.