Evidence map›Paper›PMID 10454545›Full record

ArticleMolecular and cellular biology1999

Phosphorylation-independent inhibition of Cdc28p by the tyrosine kinase Swe1p in the morphogenesis checkpoint.

J N McMillan, R A Sia, E S Bardes, D J Lew

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.7field-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

42 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
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  11. Cell cycle checkpoint regulators reach a zillion.Cell cycle (Georgetown, Tex.) · 2013
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Hsp90 phosphorylation, Wee1 and the cell cycle.Cell cycle (Georgetown, Tex.) · 2010
    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 1 institution in 1 country.

J N McMillanDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
R A Sia
E S Bardes
D J Lew
Duke Medical Center · US

Funding

CELL CYCLE CHECKPOINT THAT MONITORS MORPHOGENESISR01GM053050 · NIGMS · DUKE UNIVERSITY · PI LEW, DANIEL J · 1995 to 2012
$4.0M
MORPHOGENESIS CELL CYCLE CHECKPOINT IN BUDDING YEASTF32GM018455 · NIGMS · DUKE UNIVERSITY · PI MC MILLAN, JOHN N · 1996 to 1997
–
NIGMS NIH HHS F32 GM018455NIGMS NIH HHS GM18455NIGMS NIH HHS GM53050NIGMS NIH HHS R01 GM053050
6 · The paper itself

Abstract

The morphogenesis checkpoint in budding yeast delays cell cycle progression in G(2) when the actin cytoskeleton is perturbed, providing time for cells to complete bud formation prior to mitosis. Checkpoint-induced G(2) arrest involves the inhibition of the master cell cycle regulatory cyclin-dependent kinase, Cdc28p, by the Wee1 family kinase Swe1p. Results of experiments using a nonphosphorylatable CDC28(Y19F) allele suggested that the checkpoint stimulated two inhibitory pathways, one that promoted phosphorylation at tyrosine 19 (Y19) and a poorly characterized second pathway that did not require Cdc28p Y19 phosphorylation. We present the results from a genetic screen for checkpoint-defective mutants that led to the repeated isolation of the dominant CDC28(E12K) allele that is resistant to Swe1p-mediated inhibition. Comparison of this allele with the nonphosphorylatable CDC28(Y19F) allele suggested that Swe1p is still able to inhibit CDC28(Y19F) in a phosphorylation-independent manner and that both the Y19 phosphorylation-dependent and -independent checkpoint pathways in fact reflect Swe1p inhibition of Cdc28p. Remarkably, we found that a Swe1p mutant lacking catalytic activity could significantly delay the cell cycle in vivo during a physiological checkpoint response, even when expressed at single copy. The finding that a Wee1 family kinase expressed at physiological levels can inhibit a nonphosphorylatable cyclin-dependent kinase has broad implications for many checkpoint studies using such mutants in other organisms.

Indexed as

Cell CycleAllelesBase SequenceCDC28 Protein Kinase, S cerevisiaeCell Cycle ProteinsDNA PrimersG2 PhaseGenes, FungalMutationPhosphorylationProtein-Tyrosine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCDC28 Protein Kinase, S cerevisiaeCell Cycle ProteinsDNA PrimersProtein-Tyrosine KinasesSaccharomyces cerevisiae ProteinsSWE1 protein, S cerevisiae

Identifiers

PMID10454545
PMCPMC84473
OpenAlexW2131386971

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.