Evidence map›Paper›PMID 28130843›Full record

ArticleMolecular microbiology2017

Insufficient levels of the nrdAB-encoded ribonucleotide reductase underlie the severe growth defect of the Δhda E. coli strain.

Vignesh M P Babu, Mark Itsko, Jamie C Baxter, Roel M Schaaper, Mark D Sutton

Abstract read
In one paragraph

Article in Molecular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
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  9. Elevated Levels of the Escherichia coliJournal of bacteriology · 2021
    Article
  10. The Mutant βJournal of bacteriology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Review
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  16. Article
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  19. Review
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.

Vignesh M P BabuDepartment of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Mark ItskoGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Jamie C BaxterDepartment of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.
Roel M SchaaperGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Mark D SuttonDepartment of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.ORCID http://orcid.org/0000-0002-8221-9297

Funding

Mechanisms Of E. coli Replication FidelityZIAES065086 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SCHAAPER, ROELAND · 2009 to 2025
$7.4M
Regulation of DNA Replication and RepairR01GM066094 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SUTTON, MARK D. · 2003 to 2016
$4.0M
MECHANISMS OF E COLI REPLICATION FIDELITYZ01ES065086 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SCHAAPER, ROELAND · 1996 to 2008
$649k
Intramural NIH HHS Z01 ES065086NIGMS NIH HHS R01 GM066094
6 · The paper itself

Abstract

The ATP-bound form of the Escherichia coli DnaA replication initiator protein remodels the chromosomal origin of replication, oriC, to load the replicative helicase. The primary mechanism for regulating the activity of DnaA involves the Hda and β clamp proteins, which act together to dramatically stimulate the intrinsic DNA-dependent ATPase activity of DnaA via a process termed Regulatory Inactivation of DnaA. In addition to hyperinitiation, strains lacking hda function also exhibit cold sensitive growth at 30°C. Strains impaired for the other regulators of initiation (i.e., ΔseqA or ΔdatA) fail to exhibit cold sensitivity. The goal of this study was to gain insight into why loss of hda function impedes growth. We used a genetic approach to isolate 9 suppressors of Δhda cold sensitivity, and characterized the mechanistic basis by which these suppressors alleviated Δhda cold sensitivity. Taken together, our results provide strong support for the view that the fundamental defect associated with Δhda is diminished levels of DNA precursors, particularly dGTP and dATP. We discuss possible mechanisms by which the suppressors identified here may regulate dNTP pool size, as well as similarities in phenotypes between the Δhda strain and hda

Indexed as

Adenosine TriphosphatasesAllelesCold TemperatureDeoxyadenine NucleotidesDNA, BacterialDNA-Binding ProteinsDNA HelicasesDNA ReplicationEscherichia coliEscherichia coli ProteinsRibonucleoside Diphosphate ReductaseTrans-Activators2'-deoxyadenosine triphosphateAdenosine TriphosphatasesDeoxyadenine NucleotidesDNA, BacterialDNA-Binding ProteinsDNA HelicasesEscherichia coli ProteinsNrdA protein, E colireplication initiator proteinRibonucleoside Diphosphate ReductaseTrans-Activators

Identifiers

PMID28130843
PMCPMC5397354

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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.