Home | Sources Directory | News Releases | Calendar | Articles | RSS Sources Select News RSS Feed | Contact |  

Mating of yeast

The yeast Saccharomyces cerevisiae is a simple single celled eukaryote with both a diploid and haploid mode of existence. The mating of yeast only occurs between haploids, which can be either the a or î� (alpha) mating type and thus display simple sexual differentiation. Mating type is determined by a single locus, MAT, which in turn governs the sexual behaviour of both haploid and diploid cells. Through a form of genetic recombination, haploid yeast can switch mating type as often as every cell cycle.


[edit] Mating type and the life cycle of Saccharomyces cerevisiae

S. cerevisiae (yeast) can stably exist as either a diploid or a haploid. Both haploid and diploid yeast cells reproduce by mitosis, with daughter cells budding off of mother cells. Haploid cells are capable of mating with other haploid cells of the opposite mating type (an a cell can only mate with an î� cell, and vice versa) to produce a stable diploid cell. Diploid cells, usually upon facing stressful conditions such as nutrient depletion, can undergo meiosis to produce four haploid spores: two a spores and two î� spores.

[edit] Differences between a and î� cells

Two haploid yeast of opposite mating types secrete pheromones, grow projections and mate.

a cells produce 'a-factor', a mating pheromone which signals the presence of an a cell to neighbouring î� cells. a cells respond to î�-factor, the î� cell mating pheromone, by growing a projection (known as a shmoo) towards the source of î�-factor. Similarly, î� cells produce î�-factor, and respond to a-factor by growing a projection towards the source of the pheromone. The response of haploid cells only to the mating pheromones of the opposite mating type allows mating between a and î� cells, but not between cells of the same mating type.

These phenotypic differences between a and î� cells are due to a different set of genes being actively transcribed and repressed in cells of the two mating types. a cells activate genes which produce a-factor and produce a cell surface receptor (Ste2) which binds to î�-factor and triggers signaling within the cell. a cells also repress the genes associated with being an î� cell. Similarly, î� cells activate genes which produce î�-factor and produce a cell surface receptor (Ste3) which binds and responds to a-factor, and î� cells repress the genes associated with being an a cell.

The different sets of transcriptional repression and activation which characterize a and î� cells are caused by the presence of one of two alleles of a locus called MAT: MATa or MATî�. The MATa allele of MAT encodes a gene called a1, which in haploids direct the transcription of the a-specific transcriptional program (such as expressing STE2 and repressing STE3) which defines an a cell. The MATî� allele of MAT encodes the î�1 and î�2 genes, which in haploids direct the transcription of the î�-specific transcriptional program (such as expressing STE3, repressing STE2) which causes the cell to be an î� cell.

[edit] Differences between haploid and diploid cells

Haploid cells are one of two mating types (a or î�), and respond to the mating pheromone produced by haploid cells of the opposite mating type, and can mate with cells of the opposite mating type. Haploid cells cannot undergo meiosis. Diploid cells do not produce or respond to either mating pheromone and do not mate, but can undergo meiosis to produce four haploid cells.

Like the differences between haploid a and î� cells, different patterns of gene repression and activation are responsible for the phenotypic differences between haploid and diploid cells. In addition to the specific a and î� transcriptional patterns, haploid cells of both mating types share a haploid transcriptional pattern which activates haploid-specific genes (such as HO) and represses diploid-specific genes (such as IME1). Similarly, diploid cells activate diploid-specific genes and repress haploid-specific genes.

The different gene expression patterns of haploids and diploids are again due to the MAT locus. Haploid cells only contain one copy of each of the 16 chromosomes and thus can only possess one allele of MAT (either MATa or MATî�), which determines their mating type. Diploid cells result from the mating of an a cell and an î� cell, and thus possess 32 chromosomes (in 16 pairs), including one chromosome bearing the MATa allele and another chromosome bearing the MATî� allele. The combination of the information encoded by the MATa allele (the a1 gene) and the MATî� allele (the î�1 and î�2 genes) triggers the diploid transcriptional program. Similarly, the presence of only a single allele of MAT, whether it is MATa or MATî�, triggers the haploid transcriptional program.

The alleles present at the MAT locus are sufficient to program the mating behaviour of the cell. For example, using genetic manipulations, a MATa allele can be added to a MATî� haploid cell. Despite having a haploid complement of chromosomes, the cell now has both the MATa and MATî� alleles, and will behave like a diploid cell: it will not produce or respond to mating pheromones, and when starved will attempt to undergo meiosis, with fatal results. Similarly, deletion of one copy of the MAT locus in a diploid cell, leaving only a single MATa or MATî� allele, will cause a cell with a diploid complement of chromosomes to behave like a haploid cell.

[edit] Mating type switching

A haploid yeast dividing and undergoing a mating type switch, allowing mating and diploid formation.

Wild type haploid yeast are capable of switching mating type between a and î�. Consequently, even if a single haploid cell of a given mating type founds a colony of yeast, mating type switching will cause cells of both a and î� mating types to be present in the population. Combined with the strong drive for haploid cells to mate with cells of the opposite mating type and form diploids, mating type switching and consequent mating will cause the majority of cells in a colony to be diploid, regardless of whether a haploid or diploid cell founded the colony. The vast majority of yeast strains studied in laboratories have been altered such that they cannot perform mating type switching (by deletion of the HO gene; see below); this allows the stable propagation of haploid yeast, as haploid cells of the a mating type will remain a cells (and î� cells will remain î� cells), and will not form diploids.

Location of the silent HML and HMR loci and the active MAT locus on yeast chromosome III.

[edit] HML and HMR: the silent mating cassettes

Haploid yeast switch mating type by replacing the information present at the MAT locus. For example, an a cell will switch to an î� cell by replacing the MATa allele with the MATî� allele. This replacement of one allele of MAT for the other is possible because yeast cells carry an additional silenced copy of both the MATa and MATî� alleles: the HML (Hidden MAT Left) locus typically carries a silenced copy of the MATî� allele, and the HMR (Hidden MAT Right) locus typically carries a silenced copy of the MATa allele. The silent HML and HMR loci are often referred to as the silent mating cassettes, as the information present there is 'read into' the active MAT locus.

These additional copies of the mating type information do not interfere with the function of whatever allele is present at the MAT locus because they are not expressed, so a haploid cell with the MATa allele present at the active MAT locus is still an a cell, despite also having a (silenced) copy of the MATî� allele present at HML. Only the allele present at the active MAT locus is transcribed, and thus only the allele present at MAT will influence cell behaviour.

[edit] Mechanics of the mating type switch

Yeast mating type promoter structure

The process of mating type switching is a gene conversion event initiated by the HO gene. The HO gene is a tightly regulated haploid-specific gene that is only activated in haploid cells during the G1 phase of the cell cycle. The protein encoded by the HO gene is a DNA endonuclease, which physically cleaves DNA, but only at the MAT locus (due to the DNA sequence specificity of the HO endonuclease).

Once HO cuts the DNA at MAT, exonucleases are attracted to the cut DNA ends and begin to degrade the DNA on both sides of the cut site. This DNA degradation by exonucleases eliminates the DNA which encoded the MAT allele; however, the resulting gap in the DNA is repaired by copying in the genetic information present at either HML or HMR, filling in a new allele of either the MATa or MATî� gene. Thus, the silenced alleles of MATa and MATî� present at HML and HMR serve as a source of genetic information to repair the HO-induced DNA damage at the active MAT locus. The cells prefere to change the mating type, i.e. a MATa cell will rather use HMRî� to fill the gap thus become MATî� and vice versa. The mechanism for this specificity is unknown.

[edit] Directionality of the mating type switch

Interestingly, the repair of the MAT locus after cutting by the HO endonuclease almost always results in a mating type switch. When an a cell cuts the MATa allele present at the MAT locus, the cut at MAT will almost always be repaired by copying the information present at HML. This results in MAT being repaired to the MATî� allele, switching the mating type of the cell from a to î�. Similarly, an î� cell which has its MATî� allele cut by the HO endonuclease will almost always repair the damage using the information present at HMR, copying the MATa gene to the MAT locus and switching the mating type to a.

This is the result of the action of a recombination enhancer (RE) [1] located on the left arm of chromosome III. Deletion of this region causes a cells to incorrectly repair using HMR. In a cells, Mcm1 binds to the RE and promotes recombination of the HML region. In î� cells, the î�2 factor binds at the RE and establishes a repressive domain over RE such that recombination is unlikely to occur. An innate bias means that the default behaviour is repair from HMR. The exact mechanisms of these interactions are still under investigation.

[edit] References

  1. ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470794/pdf/15082540.pdf
  • Matthew P Scott, Paul Matsudaira, Harvey Lodish, James Darnell, Lawrence Zipursky, Chris A Kaiser, Arnold Berk, Monty Krieger (2004). Molecular Cell Biology, Fifth Edition. WH Freeman and Col, NY. ISBN 0-7167-4366-3. 

[edit] External links

Related Articles & Resources

Sources Subject Index - Experts, Sources, Spokespersons

Sources Select Resources Articles

This article is based on one or more articles in Wikipedia, with modifications and additional content by SOURCES editors. This article is covered by a Creative Commons Attribution-Sharealike 3.0 License (CC-BY-SA) and the GNU Free Documentation License (GFDL). The remainder of the content of this website, except where otherwise indicated, is copyright SOURCES and may not be reproduced without written permission. (For information use the Contact form.)

SOURCES.COM is an online portal and directory for journalists, news media, researchers and anyone seeking experts, spokespersons, and reliable information resources. Use SOURCES.COM to find experts, media contacts, news releases, background information, scientists, officials, speakers, newsmakers, spokespeople, talk show guests, story ideas, research studies, databases, universities, associations and NGOs, businesses, government spokespeople. Indexing and search applications by Ulli Diemer and Chris DeFreitas.

For information about being included in SOURCES as a expert or spokesperson see the FAQ or use the online membership form. Check here for information about becoming an affiliate. For partnerships, content and applications, and domain name opportunities contact us.

Sources home page