Evidence map›Paper›PMID 25993347›Full record

ArticlePloS one2015

Functions that Protect Escherichia coli from Tightly Bound DNA-Protein Complexes Created by Mutant EcoRII Methyltransferase.

Morgan L Henderson, Kenneth N Kreuzer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Structure ofProceedings of the National Academy of Sciences of the United States of America · 2024
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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

2 authors at 2 institutions in 1 country.

Morgan L HendersonUniversity Program in Genetics and Genomics, Duke University Medical Center, Durham NC, 27710, United States of America.
Kenneth N KreuzerUniversity Program in Genetics and Genomics, Duke University Medical Center, Durham NC, 27710, United States of America; Department of Biochemistry, Duke University Medical Center, Durham NC, 27710, United States of America.
Duke Medical Center · USDuke University · US

Funding

Genetics Training Grant-Year 26T32GM007754 · NIGMS · DUKE UNIVERSITY · PI HAASE, STEVEN B · 1985 to 2019
$8.3M
Medical Genetics Training GrantT32GM007454 · NIGMS · UNIVERSITY OF WASHINGTON · PI Gail Pairitz Jarvik, Andrew Ben Stergachis · 1985 to 2026
$6.9M
Processing and consequences of DNA-protein crosslinks in E. coliR01GM072089 · NIGMS · DUKE UNIVERSITY · PI KREUZER, KENNETH N · 2004 to 2012
$2.5M
NIGMS NIH HHS 5T32-GM007454NIGMS NIH HHS GM72089NIGMS NIH HHS R01 GM072089NIGMS NIH HHS T32 GM007454NIGMS NIH HHS T32 GM007754
6 · The paper itself

Abstract

Expression of mutant EcoRII methyltransferase protein (M.EcoRII-C186A) in Escherichia coli leads to tightly bound DNA-protein complexes (TBCs), located sporadically on the chromosome rather than in tandem arrays. The mechanisms behind the lethality induced by such sporadic TBCs are not well studied, nor is it clear whether very tight binding but non-covalent complexes are processed in the same way as covalent DNA-protein crosslinks (DPCs). Using 2D gel electrophoresis, we found that TBCs induced by M.EcoRII-C186A block replication forks in vivo. Specific bubble molecules were detected as spots on the 2D gel, only when M.EcoRII-C186A was induced, and a mutation that eliminates a specific EcoRII methylation site led to disappearance of the corresponding spot. We also performed a candidate gene screen for mutants that are hypersensitive to TBCs induced by M.EcoRII-C186A. We found several gene products necessary for protection against these TBCs that are known to also protect against DPCs induced with wild-type M.EcoRII (after 5-azacytidine incorporation): RecA, RecBC, RecG, RuvABC, UvrD, FtsK, XerCD and SsrA (tmRNA). In contrast, the RecFOR pathway and Rep helicase are needed for protection against TBCs but not DPCs induced by M.EcoRII. We propose that stalled fork processing by RecFOR and RecA promotes release of tightly bound (but non-covalent) blocking proteins, perhaps by licensing Rep helicase-driven dissociation of the blocking M.EcoRII-C186A. Our studies also argued against the involvement of several proteins that might be expected to protect against TBCs. We took the opportunity to directly compare the sensitivity of all tested mutants to two quinolone antibiotics, which target bacterial type II topoisomerases and induce a unique form of DPC. We uncovered rep, ftsK and xerCD as novel quinolone hypersensitive mutants, and also obtained evidence against the involvement of a number of functions that might be expected to protect against quinolones.

Indexed as

MutationAnti-Bacterial AgentsChromosomes, BacterialDNA, BacterialDNA-Cytosine MethylasesDNA ReplicationEscherichia coliEscherichia coli ProteinsQuinolonesRecombination, GeneticAnti-Bacterial AgentsDNA, BacterialDNA-Cytosine MethylasesDNA modification methylase EcoRIIEscherichia coli ProteinsQuinolones

Identifiers

PMID25993347
PMCPMC4437897
OpenAlexW243329329

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.