Evidence map›Paper›PMID 21357484›Full record

ArticleJournal of bacteriology2011

Single-gene deletion mutants of Escherichia coli with altered sensitivity to bicyclomycin, an inhibitor of transcription termination factor Rho.

Lillian Tran, Joshua A van Baarsel, Robert S Washburn, Max E Gottesman, Jeffrey H Miller

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. A How-To Guide for Mode of Action Analysis of Antimicrobial Peptides.Frontiers in cellular and infection microbiology · 2020
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Regulation of Transcript Elongation.Annual review of microbiology · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Lillian TranDepartment of Microbiology, Immunology, and Molecular Genetics, and the Molecular Biology Institute, University of California, and the David Geffen School of Medicine, Los Angeles, California 90095, USA.
Joshua A van Baarsel
Robert S Washburn
Max E Gottesman
Jeffrey H Miller
Columbia University Irving Medical Center · US

Funding

CONTROL OF TRANSCRIPTION TERMINATION IN E. COLIR01GM037219 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GOTTESMAN, MAX ELLIOT · 1986 to 2017
$6.6M
Control of Transcription Termination in E. coliR56GM037219 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOTTESMAN, MAX ELLIOT · 2009 to 2009
$399k
NIEHS NIH HHS ES0110875NIGMS NIH HHS GM37219NIGMS NIH HHS R01 GM037219NIGMS NIH HHS R56 GM037219
6 · The paper itself

Abstract

We have screened the entire KEIO collection of 3,985 single-gene knockouts in Escherichia coli for increased susceptibility or resistance to the antibiotic bicyclomycin (BCM), a potent inhibitor of the transcription termination factor Rho. We also compared the results to those of a recent study we conducted with a large set of antibiotics (A. Liu et al., Antimicrob. Agents Chemother. 54:1393-1403, 2010). We find that deletions of many different types of genes increase sensitivity to BCM. Some of these are involved in multidrug sensitivity/resistance, whereas others are specific for BCM. Mutations in a number of DNA recombination and repair genes increase BCM sensitivity, indicating that DNA damage leading to single- and double-strand breaks is a downstream effect of Rho inhibition. MDS42, which is deleted for all cryptic prophages and insertion elements (G. Posfai et al., Science 312:1044-1046, 2006), or W3102 deleted for the rac prophage-encoded kil gene, are partially resistant to BCM (C. J. Cardinale et al., Science 230:935-938, 2008). Deletion of cryptic prophages also overcomes the increased BCM sensitivity in some but not all mutants examined here. Deletion of the hns gene renders the cell more sensitive to BCM even in the Δkil or MDS42 background. This suggests that BCM activates additional modes of cell death independent of Kil and that these could provide a target to potentiate BCM killing.

Indexed as

Anti-Bacterial AgentsBridged Bicyclo Compounds, HeterocyclicDrug Resistance, BacterialEscherichia coliGene DeletionGene Expression Regulation, BacterialProphagesRho FactorAnti-Bacterial AgentsbicozamycinBridged Bicyclo Compounds, HeterocyclicRho Factor

Identifiers

PMID21357484
PMCPMC3133090
OpenAlexW2099067387

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.