Evidence map›Paper›PMID 11313477›Full record

ArticleMolecular and cellular biology2001

A novel form of transcriptional silencing by Sum1-1 requires Hst1 and the origin recognition complex.

A Sutton, R C Heller, J Landry, J S Choy, A Sirko, R Sternglanz

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 85 citations in OpenAlex.

  1. Systematic characterization ofFrontiers in microbiology · 2023
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Determinants of Sir2-Mediated, Silent Chromatin Cohesion.Molecular and cellular biology · 2016
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Sirtuins in epigenetic regulation.Chemical reviews · 2015
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

A SuttonDepartment of Biochemistry and Cell Biology, State University of New York, Stony Brook, New York 11794-5215, USA.
R C Heller
J Landry
J S Choy
A Sirko
R Sternglanz
Stony Brook University · USState University of New York · US

Funding

YEAST HISTONE ACETYLATION GENES AND MUTANTSR01GM055641 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI STERNGLANZ, ROLF · 1997 to 2009
$2.6M
PROTEINS AND ENZYMES AFFECTING CHROMATINR01GM028220 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI STERNGLANZ, ROLF · 1985 to 2006
$2.4M
Proteins and Enzymes Affecting ChromatinR56GM028220 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI STERNGLANZ, ROLF · 2007 to 2007
$387k
NIGMS NIH HHS GM28220NIGMS NIH HHS GM55641NIGMS NIH HHS R01 GM028220NIGMS NIH HHS R01 GM055641NIGMS NIH HHS R56 GM028220
6 · The paper itself

Abstract

In the yeast Saccharomyces cerevisiae, a and alpha mating-type information is stored in transcriptionally silenced cassettes called HML and HMR. Silencing of these loci, maintained by the formation of a specialized type of heterochromatin, requires trans-acting proteins and cis-acting elements. Proteins required for silencing include the Sir2 NAD(+)-dependent deacetylase, Sir3, and Sir4. Factors that bind to the cis elements at HMR and HML and that are important for silencing include the origin recognition complex (ORC). Mutations of any of these Sir proteins or combinations of cis elements result in loss of silencing. SUM1-1 was previously identified as a dominant mutation that restores silencing to HMR in the absence of either the Sir proteins or some of the cis elements. We have investigated the novel mechanism whereby Sum1-1 causes Sir-independent silencing at HMR and present the following findings: Sum1-1 requires the Sir2 homolog, Hst1, for silencing and most probably requires the NAD(+)-dependent deacetylase activity of this protein. Sum1-1 interacts strongly with ORC, and this strong interaction is dependent on HMR DNA. Furthermore, ORC is required for Sum1-1-mediated silencing at HMR. These observations lead to a model for Sum1-1 silencing of HMR in which Sum1-1 is recruited to HMR by binding to ORC. Sum1-1, in turn, recruits Hst1. Hst1 then deacetylates histones or other chromatin-associated proteins to cause chromatin condensation and transcriptional silencing.

Indexed as

Histone DeacetylasesSaccharomyces cerevisiae ProteinsSirtuinsFungal ProteinsGene Expression Regulation, FungalNuclear ProteinsRepressor ProteinsSaccharomyces cerevisiaeSirtuin 2Transcriptional ActivationFungal ProteinsHistone DeacetylasesHST1 protein, S cerevisiaeNuclear ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsSirtuin 2SirtuinsSUM1 protein, S cerevisiae

Identifiers

PMID11313477
PMCPMC100273
OpenAlexW2127759364

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.