Evidence map›Paper›PMID 25602519›Full record

ArticleCell cycle (Georgetown, Tex.)2015

CDC28 phosphorylates Cac1p and regulates the association of chromatin assembly factor I with chromatin.

Daniel C B Jeffery, Naoko Kakusho, Zhiying You, Marlene Gharib, Brandon Wyse, Erin Drury, Michael Weinreich, Pierre Thibault, Alain Verreault, Hisao Masai and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Cell division cycle 7 kinase is a negative regulator of cell-mediated collagen degradation.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. 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

11 authors at 4 institutions in 3 countries.

Daniel C B Jefferya Department of Molecular and Cellular Biology ; University of Guelph ; Guelph , Ontario , Canada.
Naoko Kakusho
Zhiying You
Marlene Gharib
Brandon Wyse
Erin Drury
Michael Weinreich
Pierre Thibault
Alain Verreault
Hisao Masai
Krassimir Yankulov
University of Guelph · CAInstitute for Research in Immunology and Cancer · CATokyo Metropolitan Institute of Medical Science · JPVan Andel Institute · US

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Chromatin Assembly Factor I (CAF-I) plays a key role in the replication-coupled assembly of nucleosomes. It is expected that its function is linked to the regulation of the cell cycle, but little detail is available. Current models suggest that CAF-I is recruited to replication forks and to chromatin via an interaction between its Cac1p subunit and the replication sliding clamp, PCNA, and that this interaction is stimulated by the kinase CDC7. Here we show that another kinase, CDC28, phosphorylates Cac1p on serines 94 and 515 in early S phase and regulates its association with chromatin, but not its association with PCNA. Mutations in the Cac1p-phosphorylation sites of CDC28 but not of CDC7 substantially reduce the in vivo phosphorylation of Cac1p. However, mutations in the putative CDC7 target sites on Cac1p reduce its stability. The association of CAF-I with chromatin is impaired in a cdc28-1 mutant and to a lesser extent in a cdc7-1 mutant. In addition, mutations in the Cac1p-phosphorylation sites by both CDC28 and CDC7 reduce gene silencing at the telomeres. We propose that this phosphorylation represents a regulatory step in the recruitment of CAF-I to chromatin in early S phase that is distinct from the association of CAF-I with PCNA. Hence, we implicate CDC28 in the regulation of chromatin reassembly during DNA replication. These findings provide novel mechanistic insights on the links between cell-cycle regulation, DNA replication and chromatin reassembly.

Indexed as

Amino Acid SequenceCDC28 Protein Kinase, S cerevisiaeCell Cycle ProteinsChromatinChromatin Assembly and DisassemblyChromatin Assembly Factor-1DNA ReplicationGene SilencingMolecular Sequence DataMutationPhosphorylationProliferating Cell Nuclear AntigenProtein BindingProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCDC28 Protein Kinase, S cerevisiaeCDC7 protein, S cerevisiaeCell Cycle ProteinsChromatinChromatin Assembly Factor-1Proliferating Cell Nuclear AntigenProtein Serine-Threonine KinasesRLF2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsCAC1, the largest subunit of CAF-ICAF-I, Chromatin Assembly Factor ICdc28pCDK, Cyclin-Dependent KinaseCell cycleChromatin Assembly Factor I (CAF-I)Cyclin-Dependent Kinase 8 (CDK8)Dbf4-Dependent Kinase (DDK)DDK, Dbf4-Dependent Kinase, Cdc7p-Dbf4pPCNA, Proliferating Cell Nuclear Antigen, POL30PIP, PCNA Interaction PeptideProliferating Cell Nuclear Antigen (PCNA)Telomere Position EffectTPE

Identifiers

PMID25602519
PMCPMC4352963
OpenAlexW2016781835

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.