Evidence map›Paper›PMID 27198228›Full record

ArticleGenes & development2016

Histone H3K4 methylation regulates deactivation of the spindle assembly checkpoint through direct binding of Mad2.

Andria Schibler, Evangelia Koutelou, Junya Tomida, Marenda Wilson-Pham, Li Wang, Yue Lu, Alexa Parra Cabrera, Renee J Chosed, Wenqian Li, Bing Li and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Combined TRIP13 and Aurora Kinase Inhibition Induces Apoptosis in Human Papillomavirus-Driven Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
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  13. Article
  14. Docking ofOncotarget · 2017
    Article
  15. Article
  16. Article
  17. 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

13 authors at 4 institutions in 1 country.

Andria SchiblerProgram in Genes and Development, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; The Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Center for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Evangelia KoutelouCenter for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Junya TomidaDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Center for Environmental and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Marenda Wilson-PhamThe University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Li WangThe Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Center for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Program in Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Smithville, Texas 78957, USA;
Yue LuDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Alexa Parra CabreraDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Renee J ChosedThe University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Wenqian LiThe Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Center for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Program in Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Smithville, Texas 78957, USA;
Bing LiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Xiaobing ShiProgram in Genes and Development, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; The Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Center for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Richard D WoodThe Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Center for Environmental and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Program in Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Smithville, Texas 78957, USA;
Sharon Y R DentThe Graduate School of Biomedical Sciences (GSBS) at Houston, Houston, Texas 77030, USA; Center for Cancer Epigenetics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Department of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA; Program in Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Smithville, Texas 78957, USA;
The University of Texas MD Anderson Cancer Center · USThe Graduate Center, CUNY · USHouston Graduate School of Theology · USThe University of Texas Southwestern Medical Center · US

Funding

MOLECULAR BASIS OF DIFFERENTIATION AND DEVELOPMENTT32HD007325 · NICHD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KLEIN, WILLIAM H. · 1986 to 2011
$2.1M
Function of REV3L in limiting oncogenesis via DNA damage toleranceR01CA132840 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOOD, RICHARD D · 2009 to 2013
$1.6M
Mechanisms for chromatin modification during transcription elongationR01GM090077 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI LI, BING · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA132840NICHD NIH HHS T32 HD007325NIGMS NIH HHS R01 GM090077
6 · The paper itself

Abstract

Histone H3 methylation on Lys4 (H3K4me) is associated with active gene transcription in all eukaryotes. In Saccharomyces cerevisiae, Set1 is the sole lysine methyltransferase required for mono-, di-, and trimethylation of this site. Although H3K4me3 is linked to gene expression, whether H3K4 methylation regulates other cellular processes, such as mitosis, is less clear. Here we show that both Set1 and H3K4 mutants display a benomyl resistance phenotype that requires components of the spindle assembly checkpoint (SAC), including Bub3 and Mad2. These proteins inhibit Cdc20, an activator of the anaphase-promoting complex/cyclosome (APC/C). Mutations in Cdc20 that block Mad2 interactions suppress the benomyl resistance of both set1 and H3K4 mutant cells. Furthermore, the HORMA domain in Mad2 directly binds H3, identifying a new histone H3 "reader" motif. Mad2 undergoes a conformational change important for execution of the SAC. We found that the closed (active) conformation of both yeast and human Mad2 is capable of binding methylated H3K4, but, in contrast, the open (inactive) Mad2 conformation limits interaction with methylated H3. Collectively, our data indicate that interactions between Mad2 and H3K4 regulate resolution of the SAC by limiting closed Mad2 availability for Cdc20 inhibition.

Indexed as

BenomylCdc20 ProteinsDrug ResistanceHistone-Lysine N-MethyltransferaseHistonesHumansMad2 ProteinsMethylationM Phase Cell Cycle CheckpointsMutationProtein BindingProtein ConformationRecombinant ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpindle ApparatusBenomylCdc20 ProteinsHistone-Lysine N-MethyltransferaseHistonesMad2 ProteinsRecombinant ProteinsSaccharomyces cerevisiae ProteinsSET1 protein, S cerevisiaeTubulin ModulatorschromatinH3K4HORMA domainlysine methylationSet1spindle assembly checkpoint

Identifiers

PMID27198228
PMCPMC4888839
OpenAlexW2400581115

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.