Ubiquitin-dependent degradation of the yeast Matα2 repressor enables a switch in developmental state

Jeffrey D Laney, Mark Hochstrasser

Research output: Contribution to journalArticle

34 Citations (Scopus)

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 Matα2, 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 α2 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.

Original languageEnglish (US)
Pages (from-to)2259-2270
Number of pages12
JournalGenes and Development
Volume17
Issue number18
DOIs
StatePublished - Sep 15 2003
Externally publishedYes

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Ubiquitin
Yeasts
Proteolysis
Eukaryotic Cells
Cell Lineage
Epigenomics
Phenotype

Keywords

  • Differentiation
  • Mating-type switching
  • Protein degradation
  • Saccharomyces cerevisiae

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

Cite this

Ubiquitin-dependent degradation of the yeast Matα2 repressor enables a switch in developmental state. / Laney, Jeffrey D; Hochstrasser, Mark.

In: Genes and Development, Vol. 17, No. 18, 15.09.2003, p. 2259-2270.

Research output: Contribution to journalArticle

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