Yeast Mating Type

Abstract

Mating type in baker's yeast, , has been extensively studied as a model system for cell fate determination, gene regulation, chromosome structure and genetic recombination. This work has shown that mating type is determined by alleles of a single genetic locus that codes for regulatory proteins governing genes encoding mating pheromones, pheromone receptors and downstream effectors controlling cell type. Some yeast strains are capable of switching mating type, a process involving gene replacement by information transferred from silenced copies of the mating‐type locus found elsewhere in the genome. A combination of genetic, molecular and biochemical approaches has elucidated the mechanisms of silencing and mating‐type switching and has shown them to involve processes that are conserved throughout the eukaryotic kingdom.

Key Concepts

  • Mating type in baker's yeast is determined by alleles of a single gene.
  • Products of the mating‐type locus are regulatory proteins that interact to control transcription at multiple other loci that determine cell fate.
  • A genetic approach involving isolation of sterile mutants unable to mate provided the first clues to the structure and function of the mating‐type locus.
  • Mating involves production of soluble protein mating factors and membrane‐bound receptors that trigger a signal transduction cascade upon binding of mating factor to receptor.
  • Mating is coordinated with progression through the yeast cell cycle.
  • Yeast can exist as either haploid or diploid cells with one or two sets of chromosomes; haploids can mate to form diploids.
  • Some yeast strains are homothallic and can switch mating type.
  • Mating‐type switching involves silent copies of the mating‐type locus and a site‐specific endonuclease that directs recombination between the active mating‐type locus and one of the silent copies.
  • The silent copies of the mating‐type locus are present in a heterochromatin‐like configuration that prevents their expression.
  • General recombination functions are required for mating‐type switching.

Keywords: mating type; sterile mutants; mating‐type switching; cell cycle; signal transduction, chromatin structure, homothallism

Figure 1. Genes active at the mating‐type locus in a or α haploids or in a/α diploids. The different colours indicate that there is a portion of this locus that is not the same in the two mating types. (a) In mating type a cells, the a1 gene is expressed. a‐specific genes are expressed by a default pathway, α‐specific genes are not expressed, haploid‐specific genes are expressed by default pathways and one of the haploid‐specific genes is a repressor of meiosis. (b) In mating‐type α cells, the α1 and α2 genes are both expressed. The former is an activator of α‐specific genes and the latter a repressor of a‐specific genes. Haploid‐specific genes are expressed, including the repressor of meiosis. (c) When both alleles are present in an a/α diploid, α2 protein continues to repress a‐specific genes as in (b) and interacts with the product of a1 to repress the haploid‐specific genes and allows meiosis and sporulation.
Figure 2. Signal transduction pathway for response to mating pheromone. Mating pheromone is an extracellular peptide that interacts with the extracellular portion of the appropriate transmembrane receptor (Ste2 or Ste3 protein). Binding of pheromone to receptor causes a conformational change in the associated G protein, which consists of three subunits (Gα, product of the 1 gene, Gβ, product of 4, and Gγ, product of 18). This conformational change results in dissociation of the Gβ and Gγ subunits, which activates Ste20 protein, a protein kinase. Ste20p phosphorylates the mitogen‐activated protein (MAP) kinase kinase kinase (MAPKKK), Ste11p. This in turn phosphorylates the MAP kinase kinase (MAPKK) Ste7p, which phosphorylates the MAP kinase (Fus3p). Fus3p phosphorylates target proteins that regulate the cell cycle or activate transcription of genes required for mating.
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Further Reading

Gustin MC, Albertyn J, Alexander M and Davenport K (1998) MAP kinase pathways in the yeast Saccharomyces cerevisiae. Microbiology and Molecular Biology Reviews 62: 1264–1300.

Hartwell LH (1993) Getting started in the cell cycle. In: Hall MN and Linder P, (eds). The Early Days of Yeast Genetics, pp. 307–314. Plainview, NY: Cold Spring Harbor Laboratory Press.

Hoi JWS and Dumas B (2010) Ste12 and Ste12‐like proteins, fungal transcription factors regulating development and pathogenicity. Eukaryotic Cell 9: 480–485.

Huberman LB and Murray AW (2013) Genetically engineered transvestites reveal novel mating genes in budding yeast. Genetics 195: 1277–1290.

MacKay VL (1993) a's, α's, and shmoos: mating pheromones and genetics. In: Hall MN and Linder P, (eds). The Early Days of Yeast Genetics, pp. 273–290. Plainview, NY: Cold Spring Harbor Laboratory Press.

Oshima Y (1993) Homothallism, mating‐type switching, and the controlling element model in Saccharomyces cerevisiae. In: Hall MN and Linder P, (eds). The Early Days of Yeast Genetics, pp. 291–304. Plainview, NY: Cold Spring Harbor Laboratory Press.

Saito H (2010) Regulation of cross‐talk in yeast MAPK signaling pathways. Current Opinion in Microbiology 13: 677–683.

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Montelone, Beth A(Jan 2015) Yeast Mating Type. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0000598.pub2]