Evidence map›Paper›PMID 20351295›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Cell pole-specific activation of a critical bacterial cell cycle kinase.

Antonio A Iniesta, Nathan J Hillson, Lucy Shapiro

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. 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
3.8field-weighted citation impact, top 6% 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, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Glutathione Synthesis Regulated by CtrA ProtectsFrontiers in microbiology · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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
  11. Article
  12. Article
  13. Caulobacter PopZ forms an intrinsically disordered hub in organizing bacterial cell poles.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Review
  15. Article
  16. Article
  17. Article
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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

3 authors at 1 institution in 1 country.

Antonio A IniestaDepartment of Developmental Biology, Beckman Center, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nathan J Hillson
Lucy Shapiro
Stanford University · US

Funding

REGULATION OF DIFFERENTIATION IN CAULOBACTERR01GM032506 · NIGMS · YESHIVA UNIVERSITY · PI SHAPIRO, LUCILLE · 1985 to 2014
$7.1M
DEVELOPMENT CONTROL OF DNA REPLICATION IN CAULOBACTERR01GM051426 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1994 to 2013
$3.8M
3D Chromosome/Replisome Positioning in Bacterial CellsR24GM073011 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 2005 to 2008
$1.5M
REGULATION OF DIFFERENTIATION IN CAULOBACTERR37GM032506 · NIGMS · STANFORD UNIVERSITY · PI SHAPIRO, LUCILLE · 1993 to 2002
$1.4M
NIGMS NIH HHS GM073011NIGMS NIH HHS GM32506NIGMS NIH HHS GM51426NIGMS NIH HHS R01 GM032506NIGMS NIH HHS R01 GM051426NIGMS NIH HHS R24 GM073011NIGMS NIH HHS R37 GM032506
6 · The paper itself

Abstract

Caulobacter crescentus integrates phospho-signaling pathways and transcription factor regulatory cascades to drive the cell cycle. Despite the essential role of the CckA histidine kinase in the control of cell cycle events, the factors that signal its activation at a specific time in the cell cycle have remained elusive. A conditional genetic screen for CckA mislocalization mutants, using automated fluorescence microscopy and an image processing platform, revealed that the essential DivL protein kinase promotes CckA localization, autophosphorylation, and activity at the new cell pole. The transient accumulation of DivL at the new cell pole, but not its kinase activity, is required for the localization and activation of CckA. Because DivL and CckA accumulate at the same cell pole after the initiation of DNA replication and were found to interact in vivo, we propose that DivL recruits CckA to the pole, thereby promoting its autophosphorylation and activity.

Indexed as

Gene Expression Regulation, BacterialBacterial ProteinsCaulobacter crescentusCell CycleG1 PhaseGenes, ReporterHemeproteinsHistidine KinaseMicroscopy, FluorescenceModels, BiologicalPhosphorylationProtein KinasesSignal TransductionBacterial ProteinsFixL protein, BacteriaHemeproteinsHistidine KinaseProtein Kinases

Identifiers

PMID20351295
PMCPMC2872457
OpenAlexW1988674422

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.