Evidence map›Paper›PMID 12952895›Full record

ArticleGenes & development2003

Ubiquitin-dependent degradation of the yeast Mat(alpha)2 repressor enables a switch in developmental state.

Jeffrey D Laney, Mark Hochstrasser

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Ubiquitin and proteasomes in transcription.Annual review of biochemistry · 2012
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jeffrey D LaneyDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520-8114, USA.
Mark Hochstrasser
Yale University · US

Funding

Degradation of Short Lived Regulatory Protein in YeastR37GM046904 · NIGMS · YALE UNIVERSITY · PI HOCHSTRASSER, MARK W · 2009 to 2018
$3.6M
DEGRADTION OF SHORT-LIVED REGULATORY PROTEINS IN YEASTR01GM046904 · NIGMS · YALE UNIVERSITY · PI HOCHSTRASSER, MARK W · 1992 to 2020
$3.6M
NIGMS NIH HHS GM46904NIGMS NIH HHS R01 GM046904NIGMS NIH HHS R37 GM046904
6 · The paper itself

Abstract

Developmental transitions in eukaryotic cell lineages revolve around two general processes: the dismantling of the regulatory program specifying an initial differentiated state and its replacement by a new system of regulators. However, relatively little is known about the mechanisms by which a previous regulatory state is inactivated. Protein degradation is implicated in a few examples, but the molecular reasons that a formerly used regulator must be removed are not understood. Many yeast strains undergo a developmental transition in which cells of one mating type differentiate into a distinct cell type by a programmed genetic rearrangement at the MAT locus. We find that Mat(alpha)2, a MAT-encoded transcriptional repressor that is key to creating several cell types, must be rapidly degraded for cells to switch their mating phenotype properly. Strikingly, ubiquitin-dependent proteolysis of alpha2 is required for two mechanistically distinct purposes: It allows the timely inactivation of one transcriptional repressor complex, and it prevents the de novo assembly of a different, inappropriate regulatory complex. Analogous epigenetic mechanisms for reprogramming transcription are likely to operate in many developmental pathways.

Indexed as

Genes, FungalGenes, Mating Type, FungalSaccharomyces cerevisiae ProteinsUbiquitin-Conjugating EnzymesCarrier ProteinsHomeodomain ProteinsLigasesRepressor ProteinsSaccharomyces cerevisiaeUbiquitinCarrier ProteinsHomeodomain ProteinsLigasesMATA2 protein, S cerevisiaeRepressor ProteinsSaccharomyces cerevisiae ProteinsUBC1 protein, S cerevisiaeUbiquitinUbiquitin-Conjugating Enzymes

Identifiers

PMID12952895
PMCPMC196463
OpenAlexW2135792947

What OpenQuestion holds

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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.