Evidence map›Paper›PMID 17827294›Full record

ArticleJournal of bacteriology2007

DivL performs critical cell cycle functions in Caulobacter crescentus independent of kinase activity.

Sarah J Reisinger, Sarah Huntwork, Patrick H Viollier, Kathleen R Ryan

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Analysis ofJournal of bacteriology · 2019
    Article
  7. Review
  8. Integration of cell cycle signals by multi-PAS domain kinases.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Regulated Proteolysis in Bacteria: Caulobacter.Annual review of genetics · 2016
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Microbial protein-tyrosine kinases.The Journal of biological chemistry · 2014
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 3 institutions in 1 country.

Sarah J ReisingerDepartment of Plant and Microbial Biology, University of California, Berkeley, Berkeley, California 94720, USA.
Sarah Huntwork
Patrick H Viollier
Kathleen R Ryan
University of California, Berkeley · USCase Western Reserve University · USStanford University · US

Funding

REGULATION OF DIFFERENTIATION IN CAULOBACTERR01GM032506 · NIGMS · YESHIVA UNIVERSITY · PI SHAPIRO, LUCILLE · 1985 to 2014
$7.1M
REGULATION OF DIFFERENTIATION IN CAULOBACTERR37GM032506 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1993 to 2002
$1.4M
NIGMS NIH HHS GM032506NIGMS NIH HHS R01 GM032506NIGMS NIH HHS R37 GM032506
6 · The paper itself

Abstract

The Caulobacter cell cycle is regulated by a network of two-component signal transduction proteins. Phosphorylation and stability of the master transcriptional regulator CtrA are controlled by the CckA-ChpT phosphorelay, and CckA activity is modulated by another response regulator, DivK. In a screen to identify suppressors of the cold-sensitive divK341 mutant, we found point mutations in the essential gene divL. DivL is similar to histidine kinases but has a tyrosine instead of a histidine at the conserved phosphorylation site (Y550). Surprisingly, we found that the ATPase domain of DivL is not essential for Caulobacter viability. We show that DivL selectively affects CtrA phosphorylation but not CtrA proteolysis, indicating that DivL acts in a pathway independent of the CckA-ChpT phosphorelay. divL can be deleted in a strain overproducing the phosphomimetic protein CtrAD51E, but unlike DeltactrA cells expressing CtrAD51E, this strain is profoundly impaired in the control of chromosome replication and cell division. Thus, DivL performs a second function in addition to promoting CtrA phosphorylation. DivL is required for bipolar DivK localization and positively regulates DivK phosphorylation. Our results show that DivL controls two key cell cycle regulators, CtrA and DivK, and that phosphoryl transfer is not DivL's essential cellular activity.

Indexed as

AllelesBacterial ProteinsCaulobacter crescentusCell CycleDNA-Binding ProteinsGene Expression Regulation, BacterialHistidine KinaseMutationPhosphorylationProtein KinasesProtein TransportTranscription FactorsBacterial ProteinsCtrA protein, CaulobacterDivK protein, Caulobacter crescentusDNA-Binding ProteinsHistidine KinaseProtein KinasesTranscription Factors

Identifiers

PMID17827294
PMCPMC2168681
OpenAlexW2127321623

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.