Evidence map›Paper›PMID 25349992›Full record

ArticlePLoS biology2014

Cell fate regulation governed by a repurposed bacterial histidine kinase.

W Seth Childers, Qingping Xu, Thomas H Mann, Irimpan I Mathews, Jimmy A Blair, Ashley M Deacon, Lucy Shapiro

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. TheJournal of bacteriology · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
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  20. Multilayered control of chromosome replication inBiochemical Society transactions · 2019
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

W Seth ChildersDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California, United States of America.
Qingping XuStanford Synchrotron Radiation Lightsource, SLAC National Accelerator Laboratory, Menlo Park, California, United States of America; Joint Center for Structural Genomics, United States of America.
Thomas H MannDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California, United States of America.
Irimpan I MathewsStanford Synchrotron Radiation Lightsource, SLAC National Accelerator Laboratory, Menlo Park, California, United States of America.
Jimmy A BlairDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California, United States of America.
Ashley M DeaconStanford Synchrotron Radiation Lightsource, SLAC National Accelerator Laboratory, Menlo Park, California, United States of America; Joint Center for Structural Genomics, United States of America.
Lucy ShapiroDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, California, United States of America.
Stanford University · USSLAC National Accelerator Laboratory · US

Funding

Technology Evaluation CoreU54GM074898 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI STEVENS, RAYMOND C · 2005 to 2009
$50.6M
Structure Determination Core at SSRLU54GM094586 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI WILSON, IAN A · 2010 to 2014
$40.1M
Supplement to Enhance Wellness and Resiliency in the Graduate EnvironmentT32GM007276 · NIGMS · STANFORD UNIVERSITY · PI MORRISON, ASHBY J. · 1985 to 2023
$32.9M
Subcellular architecture of regulatory protein complexes at the bacterial poleR01GM086196 · NIGMS · STANFORD UNIVERSITY · PI MOERNER, WILLIAM E, SHAPIRO, LUCILLE · 2008 to 2015
$4.7M
DEVELOPMENT CONTROL OF DNA REPLICATION IN CAULOBACTERR01GM051426 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1994 to 2013
$3.8M
NIGMS NIH HHS GM074898NIGMS NIH HHS R01 GM051426NIGMS NIH HHS R01 GM086196NIGMS NIH HHS R01 GM51426NIGMS NIH HHS T32 GM007276NIGMS NIH HHS U54 GM074898NIGMS NIH HHS U54 GM094586PHS HHS F32A1082915
6 · The paper itself

Abstract

One of the simplest organisms to divide asymmetrically is the bacterium Caulobacter crescentus. The DivL pseudo-histidine kinase, positioned at one cell pole, regulates cell-fate by controlling the activation of the global transcription factor CtrA via an interaction with the response regulator (RR) DivK. DivL uniquely contains a tyrosine at the histidine phosphorylation site, and can achieve these regulatory functions in vivo without kinase activity. Determination of the DivL crystal structure and biochemical analysis of wild-type and site-specific DivL mutants revealed that the DivL PAS domains regulate binding specificity for DivK∼P over DivK, which is modulated by an allosteric intramolecular interaction between adjacent domains. We discovered that DivL's catalytic domains have been repurposed as a phosphospecific RR input sensor, thereby reversing the flow of information observed in conventional histidine kinase (HK)-RR systems and coupling a complex network of signaling proteins for cell-fate regulation.

Indexed as

Bacterial ProteinsCaulobacter crescentusCell CycleDimerizationHistidine KinaseProtein BindingProtein KinasesProtein Structure, TertiaryBacterial ProteinsDivK protein, Caulobacter crescentusHistidine KinaseProtein Kinases

Identifiers

PMID25349992
PMCPMC4211667
OpenAlexW2018942098

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.