Evidence map›Paper›PMID 27489001›Full record

ArticleGenetics2016

Histone Deacetylases with Antagonistic Roles in Saccharomyces cerevisiae Heterochromatin Formation.

Deborah M Thurtle-Schmidt, Anne E Dodson, Jasper Rine

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Whole-Genome Sequencing of Yeast Cells.Current protocols in molecular biology · 2019
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

3 authors at 2 institutions in 1 country.

Deborah M Thurtle-SchmidtDepartment of Molecular and Cell Biology and California Institute for Quantitative Biosciences, University of California, Berkeley, California 94720.ORCID 0000-0002-9747-9585
Anne E DodsonDepartment of Molecular and Cell Biology and California Institute for Quantitative Biosciences, University of California, Berkeley, California 94720.ORCID 0000-0001-7719-0496
Jasper RineDepartment of Molecular and Cell Biology and California Institute for Quantitative Biosciences, University of California, Berkeley, California 94720 jrine@berkeley.edu.
QB3 · USUniversity of California, Berkeley · US

Funding

THE MOLECULAR BASIS OF CELL FUNCTIONT32GM007232 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BILDER, DAVID, UNAL, ELCIN · 1985 to 2022
$36.4M
GENETIC ANALYSIS OF THE GENES CONTROLLING A POSITIONR01GM031105 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RINE, JASPER D · 1985 to 2020
$6.4M
Genome Sequencer FLXS10RR029668 · NCRR · UNIVERSITY OF CALIFORNIA BERKELEY · PI NGAI, JOHN J. · 2010 to 2010
$623k
Illumina Sequencer to Facilitate Functional Genomics at BerkeleyS10RR027303 · NCRR · UNIVERSITY OF CALIFORNIA BERKELEY · PI TAYLOR, JOHN W. · 2010 to 2010
$500k
NCRR NIH HHS S10 RR027303NCRR NIH HHS S10 RR029668NIGMS NIH HHS R01 GM031105NIGMS NIH HHS T32 GM007232
6 · The paper itself

Abstract

As the only catalytic member of the Sir-protein gene-silencing complex, Sir2's catalytic activity is necessary for silencing. The only known role for Sir2's catalytic activity in Saccharomyces cerevisiae silencing is to deacetylate N-terminal tails of histones H3 and H4, creating high-affinity binding sites for the Sir-protein complex, resulting in association of Sir proteins across the silenced domain. This histone deacetylation model makes the simple prediction that preemptively removing Sir2's H3 and H4 acetyl substrates, by mutating these lysines to unacetylatable arginines, or removing the acetyl transferase responsible for their acetylation, should restore silencing in the Sir2 catalytic mutant. However, this was not the case. We conducted a genetic screen to explore what aspect of Sir2's catalytic activity has not been accounted for in silencing. Mutation of a nonsirtuin histone deacetylase, Rpd3, restored Sir-protein-based silencing in the absence of Sir2's catalytic activity. Moreover, this antagonism could be mediated by either the large or the small Rpd3-containing complex. Interestingly, this restoration of silencing appeared independent of any known histone H3 or H4 substrates of Rpd3 Investigation of Sir-protein association in the Rpd3 mutant revealed that the restoration of silencing was correlated with an increased association of Sir proteins at the silencers, suggesting that Rpd3 was an antagonist of Sir2's function in nucleation of Sir proteins to the silencer. Additionally, restoration of silencing by Rpd3 was dependent on another sirtuin family member, Hst3, indicating multiple antagonistic roles for deacetylases in S. cerevisiae silencing.

Indexed as

AcetylationChromatin Assembly and DisassemblyGene SilencingHeterochromatinHistone DeacetylasesHistonesMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSirtuin 2Transcription, GeneticHeterochromatinHistone DeacetylasesHistonesRPD3 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSirtuin 2H4K16heterochromatinHst3Rpd3Sir2

Identifiers

PMID27489001
PMCPMC5012384
OpenAlexW2497049915

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.