Evidence map›Paper›PMID 25619765›Full record

ArticleCurrent biology : CB2015

The CENP-A N-tail confers epigenetic stability to centromeres via the CENP-T branch of the CCAN in fission yeast.

H Diego Folco, Christopher S Campbell, Karen M May, Celso A Espinoza, Karen Oegema, Kevin G Hardwick, Shiv I S Grewal, Arshad Desai

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Kinetochore Architecture Employs Diverse Linker Strategies Across Evolution.Frontiers in cell and developmental biology · 2022
    Review
  6. Article
  7. The N-terminal tail ofMolecular biology of the cell · 2021
    Article
  8. International journal of molecular sciences · 2020
    Article
  9. Article
  10. Review
  11. Centromere repositioning causes inversion of meiosis and generates a reproductive barrier.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

8 authors at 4 institutions in 3 countries.

H Diego FolcoLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Laboratory of Biochemistry and Molecular Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Christopher S CampbellLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Karen M MayWellcome Trust Centre for Cell Biology, Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Celso A EspinozaLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Karen OegemaLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Kevin G HardwickWellcome Trust Centre for Cell Biology, Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK.
Shiv I S GrewalLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Arshad DesaiLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: abdesai@ucsd.edu.
University of California San Diego · USNational Cancer Institute · USWellcome Centre for Cell Biology · GBLudwig Cancer Research · BE

Funding

Roles of Chromatin-modifying Factors in Epigenetic Control of the GenomeZIABC011208 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GREWAL, SHIVINDER S · 2009 to 2025
$28.1M
Contemporary Approaches to Cancer Cell Signaling and CommunicationT32CA009523 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DONOGHUE, DANIEL J, YANG, JING · 1985 to 2025
$12.1M
Kinetochore Specification and FunctionR01GM074215 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DESAI, ARSHAD · 2005 to 2025
$8.2M
Intramural NIH HHSNCI NIH HHS T32 CA009523NCI NIH HHS T32 CA009523-27S1NIGMS NIH HHS GM074215NIGMS NIH HHS R01 GM074215Wellcome TrustWellcome Trust 083610Wellcome Trust 092076
6 · The paper itself

Abstract

In most eukaryotes, centromeres are defined epigenetically by presence of the histone H3 variant CENP-A [1-3]. CENP-A-containing chromatin recruits the constitutive centromere-associated network (CCAN) of proteins, which in turn directs assembly of the outer kinetochore to form microtubule attachments and ensure chromosome segregation fidelity [4-6]. Whereas the mechanisms that load CENP-A at centromeres are being elucidated, the functions of its divergent N-terminal tail remain enigmatic [7-12]. Here, we employ the well-studied fission yeast centromere [13-16] to investigate the function of the CENP-A (Cnp1) N-tail. We show that alteration of the N-tail does not affect Cnp1 loading at centromeres, outer kinetochore formation, or spindle checkpoint signaling but nevertheless elevates chromosome loss. N-tail mutants exhibited synthetic lethality with an altered centromeric DNA sequence, with rare survivors harboring chromosomal fusions in which the altered centromere was epigenetically inactivated. Elevated centromere inactivation was also observed for N-tail mutants with unaltered centromeric DNA sequences. N-tail mutants specifically reduced localization of the CCAN proteins Cnp20/CENP-T and Mis6/CENP-I, but not Cnp3/CENP-C. Overexpression of Cnp20/CENP-T suppressed defects in an N-tail mutant, suggesting a link between reduced CENP-T recruitment and the observed centromere inactivation phenotype. Thus, the Cnp1 N-tail promotes epigenetic stability of centromeres in fission yeast, at least in part via recruitment of the CENP-T branch of the CCAN.

Indexed as

CentromereChromatin ImmunoprecipitationChromosomal Proteins, Non-HistoneDNA PrimersElectrophoresis, Gel, Pulsed-FieldEpigenesis, GeneticFluorescenceHistonesImmunoblottingMutationPolymerase Chain ReactionSchizosaccharomycesSchizosaccharomyces pombe ProteinsChromosomal Proteins, Non-HistoneCnp1 protein, S pombeDNA PrimersHistonesSchizosaccharomyces pombe Proteins

Identifiers

PMID25619765
PMCPMC4318777
OpenAlexW2000490369

What OpenQuestion holds

Textmetadata
LicenceTDM
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.