Evidence map›Paper›PMID 19172996›Full record

ArticlePloS one2009

Whi5 regulation by site specific CDK-phosphorylation in Saccharomyces cerevisiae.

Michelle V Wagner, Marcus B Smolka, Rob A M de Bruin, Huilin Zhou, Curt Wittenberg, Steven F Dowdy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

45 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  8. TOR Complex 1: Orchestrating Nutrient Signaling and Cell Cycle Progression.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. What programs the size of animal cells?Frontiers in cell and developmental biology · 2022
    Review
  16. Article
  17. Article
  18. Cell-size regulation in budding yeast does not depend on linear accumulation of Whi5.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  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

6 authors at 4 institutions in 1 country.

Michelle V WagnerHoward Hughes Medical Institute, University of California San Diego School of Medicine, La Jolla, California, USA.
Marcus B Smolka
Rob A M de Bruin
Huilin Zhou
Curt Wittenberg
Steven F Dowdy
Ludwig Cancer Research · USScripps Research Institute · USHoward Hughes Medical Institute · USUniversity of California, San Diego · US

Funding

Training Program in Basic Clinical GeneticsT32GM008666 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMILTON, BRUCE A · 1998 to 2021
$8.6M
Predoctoral and Postdoctoral Training in Cancer Cell BiologyT32CA067754 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JEAN Y.J. WANG · 1995 to 2026
$6.5M
Regulation and functions of DNA damage checkpoint kinases in YeastR01GM080469 · NIGMS · LUDWIG INSTITUTE FOR CANCER RES LTD · PI ZHOU, HUILIN · 2007 to 2011
$1.4M
Howard Hughes Medical InstituteNCI NIH HHS CA067754NCI NIH HHS T32 CA067754NIGMS NIH HHS (GM008666NIGMS NIH HHS R01 GM080469NIGMS NIH HHS T32 GM008666
6 · The paper itself

Abstract

The Whi5 transcriptional repressor is a negative regulator of G1 cell cycle progression in Saccharomyces cerevisiae and is functionally equivalent to the Retinoblastoma (Rb) tumor suppressor protein in mammals. In early G1, Whi5 binds to and inhibits SBF (Swi4/Swi6) transcriptional complexes. At Start, Cln:Cdc28 kinases phosphorylate and inactivate Whi5, causing its dissociation from SBF promoters and nuclear export, allowing activation of SBF transcription and entry into late G1. In an analysis of Whi5 phosphorylation, we found that 10 of the 12 putative CDK phosphorylation sites on Whi5 were occupied in vivo in asynchronously growing cells. In addition, we identified 6 non-CDK Whi5 phosphorylation sites. Whi5 CDK and non-CDK phosphorylation mutants were functional and able to rescue the small cell size of whi5Delta cells. However, the Whi5 CDK mutant with all 12 putative CDK sites changed to alanine causes a dramatic cell cycle phenotype when expressed with a Swi6 CDK phosphorylation mutant. Mutational analysis of Whi5 determined that only four C-terminal CDK sites were necessary and sufficient for Whi5 inactivation when Swi6 CDK sites were also mutated. Although these four Whi5 CDK sites do not wholly determine Whi5 nuclear export, they do impact regulation of cell size. Taken together, these observations begin to dissect the regulatory role of specific phosphorylation sites on Whi5.

Indexed as

Active Transport, Cell NucleusAmino Acid SequenceCell CycleCell NucleusCyclin-Dependent KinasesDNA Mutational AnalysisKaryopherinsMolecular Sequence DataMutant ProteinsMutationPhosphorylationProtein TransportRepressor ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCyclin-Dependent KinasesKaryopherinsMSN5 protein, S cerevisiaeMutant ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsWhi5 protein, S cerevisiae

Identifiers

PMID19172996
PMCPMC2627923
OpenAlexW1966912773

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.