Evidence map›Paper›PMID 21441216›Full record

ArticleGenetics2011

Differential contributions of histone H3 and H4 residues to heterochromatin structure.

Qun Yu, Lars Olsen, Xinmin Zhang, Jef D Boeke, Xin Bi

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2011. 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
0.7field-weighted citation impact, top 31% 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, 23 citations in OpenAlex.

  1. Understanding and Simulating the Dynamics of a Polymer-Like Chromatin.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  2. Measuring the buffering capacity of gene silencing inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  3. Review
  4. Histone Tail Conformations: A Fuzzy Affair with DNA.Trends in biochemical sciences · 2021
    Review
  5. Tau Stabilizes Chromatin Compaction.Frontiers in cell and developmental biology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Proliferating cell nuclear antigen (PCNA) contributes to the high-order structure and stability of heterochromatin in Saccharomyces cerevisiae.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Epigenetics in Saccharomyces cerevisiae.Cold Spring Harbor perspectives in biology · 2013
    Review
  15. Article
  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

5 authors at 2 institutions in 2 countries.

Qun YuDepartment of Biology, University of Rochester, Rochester, New York 14627, USA.
Lars Olsen
Xinmin Zhang
Jef D Boeke
Xin Bi
University of Rochester · USHigh Throughput Biology (United States) · US

Funding

TCP5: ACTIVE SITE LABELING REAGENT FOR ACETYLTRANSFERASESU54RR020839 · NCRR · JOHNS HOPKINS UNIVERSITY · PI BOEKE, JEF D · 2004 to 2011
$27.4M
Transcriptionally silent chromatin domains in yeastR01GM062484 · NIGMS · UNIVERSITY OF ROCHESTER · PI BI, XIN · 2001 to 2009
$2.4M
NCRR NIH HHS U54 RR020839NIGMS NIH HHS GM62484NIGMS NIH HHS R01 GM062484
6 · The paper itself

Abstract

Transcriptional silencing in Saccharomyces cerevisiae is mediated by heterochromatin. There is a plethora of information regarding the roles of histone residues in transcriptional silencing, but exactly how histone residues contribute to heterochromatin structure is not resolved. We address this question by testing the effects of a series of histone H3 and H4 mutations involving residues in their aminoterminal tails, on the solvent-accessible and lateral surfaces of the nucleosome, and at the interface of the H3/H4 tetramer and H2A/H2B dimer on heterochromatin structure and transcriptional silencing. The general state, stability, and conformational heterogeneity of chromatin are examined with a DNA topology-based assay, and the primary chromatin structure is probed by micrococcal nuclease. We demonstrate that the histone mutations differentially affect heterochromatin. Mutations of lysine 16 of histone H4 (H4-K16) and residues in the LRS (loss of rDNA silencing) domain of nucleosome surface markedly alter heterochromatin structure, supporting the notion that H4-K16 and LRS play key roles in heterochromatin formation. Deletion of the aminoterminal tail of H3 moderately alters heterochromatin structure. Interestingly, a group of mutations in the globular domains of H3 and H4 that abrogate or greatly reduce transcriptional silencing increase the conformational heterogeneity and/or reduce the stability of heterochromatin without affecting its overall structure. Surprisingly, yet another series of mutations abolish or reduce silencing without significantly affecting the structure, stability, or conformational heterogeneity of heterochromatin. Therefore, histone residues may contribute to the structure, stability, conformational heterogeneity, or other yet-to-be-characterized features of heterochromatin important for transcriptional silencing.

Indexed as

AcetylationAmino AcidsAmino Acid SequenceArginineChromatinDNA, FungalGene Expression Regulation, FungalHeterochromatinHistonesLysineMethylationMolecular Sequence DataMutationNucleosomesPhosphorylationSaccharomyces cerevisiaeAmino AcidsArginineChromatinDNA, FungalHeterochromatinHistonesLysineNucleosomesSaccharomyces cerevisiae ProteinsSerine

Identifiers

PMID21441216
PMCPMC3122323
OpenAlexW2128369348

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.