Evidence map›Paper›PMID 8909534›Full record

ArticleThe Journal of cell biology1996

Activation of an MAP kinase cascade leads to Sir3p hyperphosphorylation and strengthens transcriptional silencing.

E M Stone, L Pillus

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Substrates of the MAPK Slt2: Shaping Yeast Cell Integrity.Journal of fungi (Basel, Switzerland) · 2022
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The budding yeast nucleus.Cold Spring Harbor perspectives in biology · 2010
    Review
  14. Article
  15. Article
  16. The glucanosyltransferase Gas1 functions in transcriptional silencing.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  17. Article
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

E M StoneDepartment of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder 80309-0347, USA.
L Pillus
University of Colorado Boulder · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During cell division and growth, the nucleus and chromosomes are remodeled for DNA replication and cell type-specific transcriptional control. The yeast silencing protein Sir3p functions in both chromosome structure and in transcriptional regulation. Specifically, Sir3p is critical for the maintenance of telomere structure and for transcriptional repression at both the silent mating-type loci and telomeres. We demonstrate that Sir3p becomes hyperphosphorylated in response to mating pheromone, heat shock, and starvation. Cells exposed to pheromone arrest in G1 of the cell cycle, yet G1 arrest is neither necessary nor sufficient for pheromone-induced Sir3p hyperphosphorylation. Rather, hyperphosphorylation of Sir3p requires the mitogen-activated protein (MAP) kinase pathway genes STE11, STE7, FUS3/KSS1, and STE12, indicating that an intact signal transduction pathway is crucial for this Sir3p phosphorylation event. Constitutive activation of the pheromone-response MAP kinase cascade in an STE11-4 strain leads to hyperphosphorylation of Sir3p and increased Sir3p-dependent transcriptional silencing at telomeres. Regulated phosphorylation of Sir3p may thus be a mechanistically significant means for modulating silencing. Together, these observations suggest a novel role for MAP kinase signal transduction in coordinating chromatin structure and nuclear organization for transcriptional silencing.

Indexed as

Silent Information Regulator Proteins, Saccharomyces cerevisiaeCalcium-Calmodulin-Dependent Protein KinasesEnzyme ActivationFungal ProteinsG1 PhaseGene Expression Regulation, FungalHeat-Shock ResponseMating FactorMutationPeptidesPheromonesPhosphoproteinsPhosphorylationSaccharomyces cerevisiaeSignal TransductionTelomereCalcium-Calmodulin-Dependent Protein KinasesFungal ProteinsMating FactorPeptidesPheromonesPhosphoproteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR3 protein, S cerevisiaeTrans-Activators

Identifiers

PMID8909534
PMCPMC2121063
OpenAlexW2095018331

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.