Faculty Opinions recommendation of Mating-type switching by chromosomal inversion in methylotrophic yeasts suggests an origin for the three-locus Saccharomyces cerevisiae system.

2014 ◽  
Author(s):  
Joseph Heitman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Chromosomal Inversion ◽  
Methylotrophic Yeasts ◽  
Mating Type Switching

Homothallic mating type switching generates lethal chromosome breaks in rad52 strains of Saccharomyces cerevisiae

1981 ◽  
Vol 1 (6) ◽  
pp. 522-534
Author(s):  
B Weiffenbach ◽  
J E Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Deoxyribonucleic Acid ◽  
Type Locus ◽  
Mating Type Switching ◽  
Lethal Event ◽  
Bona Fide ◽  
Chromosome Iii ◽  
Mat Locus ◽  
Type Information

In homothallic cells of Saccharomyces cerevisiae, a or alpha mating type information at the mating type locus (MAT) is replaced by the transposition of the opposite mating type allele from HML alpha or HMRa. The rad52-1 mutation, which reduces mitotic and abolishes meiotic recombination, also affects homothallic switching (Malone and Esposito, Proc. Natl. Acad. Sci. U.S.A. 77:503-507, 1980). We have found that both HO rad52 MATa and HO rad52 MAT alpha cells die. This lethality is suppressed by mutations that substantially reduce but do not eliminate homothallic conversions. These mutations map at or near the MAT locus (MAT alpha inc, MATa-inc, MATa stk1) or are unlinked to MAT (HO-1 and swi1). These results suggest that the switching event itself is involved in the lethality. With the exception of swi1, HO rad52 strains carrying one of the above mutations cannot convert mating type at all. MAT alpha rad52 HO swi1 strains apparently can switch MAT alpha to MATa. However, when we analyzed these a maters, we found that few, if any, of them were bona fide MATa cells. These a-like cells were instead either deleted for part of chromosome III distal to and including MAT or had lost the entire third chromosome. Approximately 30% of the time, an a-like cell could be repaired to a normal MATa genotype if the cell was mated to a RAD52 MAT alpha-inc strain. The effects of rad52 were also studied in mata/MAT alpha-inc rad52/rad52 ho/HO diploids. When this diploid attempted to switch mata to MATa, an unstable broken chromosome was generated in nearly every cell. These studies suggest that homothallic switching involves the formation of a double-stranded deoxyribonucleic acid break or a structure which is labile in rad52 cells and results in a broken chromosome. We propose that the production of a double-stranded deoxyribonucleic acid break is the lethal event in rad52 HO cells.

scholarly journals Homothallic mating type switching generates lethal chromosome breaks in rad52 strains of Saccharomyces cerevisiae.

1981 ◽  
Vol 1 (6) ◽  
pp. 522-534 ◽  
Author(s):  
B Weiffenbach ◽  
J E Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Deoxyribonucleic Acid ◽  
Type Locus ◽  
Mating Type Switching ◽  
Lethal Event ◽  
Bona Fide ◽  
Chromosome Iii ◽  
Mat Locus ◽  
Type Information

In homothallic cells of Saccharomyces cerevisiae, a or alpha mating type information at the mating type locus (MAT) is replaced by the transposition of the opposite mating type allele from HML alpha or HMRa. The rad52-1 mutation, which reduces mitotic and abolishes meiotic recombination, also affects homothallic switching (Malone and Esposito, Proc. Natl. Acad. Sci. U.S.A. 77:503-507, 1980). We have found that both HO rad52 MATa and HO rad52 MAT alpha cells die. This lethality is suppressed by mutations that substantially reduce but do not eliminate homothallic conversions. These mutations map at or near the MAT locus (MAT alpha inc, MATa-inc, MATa stk1) or are unlinked to MAT (HO-1 and swi1). These results suggest that the switching event itself is involved in the lethality. With the exception of swi1, HO rad52 strains carrying one of the above mutations cannot convert mating type at all. MAT alpha rad52 HO swi1 strains apparently can switch MAT alpha to MATa. However, when we analyzed these a maters, we found that few, if any, of them were bona fide MATa cells. These a-like cells were instead either deleted for part of chromosome III distal to and including MAT or had lost the entire third chromosome. Approximately 30% of the time, an a-like cell could be repaired to a normal MATa genotype if the cell was mated to a RAD52 MAT alpha-inc strain. The effects of rad52 were also studied in mata/MAT alpha-inc rad52/rad52 ho/HO diploids. When this diploid attempted to switch mata to MATa, an unstable broken chromosome was generated in nearly every cell. These studies suggest that homothallic switching involves the formation of a double-stranded deoxyribonucleic acid break or a structure which is labile in rad52 cells and results in a broken chromosome. We propose that the production of a double-stranded deoxyribonucleic acid break is the lethal event in rad52 HO cells.

scholarly journals A site-specific endonuclease essential for mating-type switching in Saccharomyces cerevisiae

Cell ◽  
1983 ◽  
Vol 35 (1) ◽  
pp. 167-174 ◽  
Author(s):  
Richard Kostriken ◽  
Jeffrey N. Strathern ◽  
Amar J.S. Klar ◽  
James B. Hicks ◽  
Fred Heffron
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Site Specific ◽  
Mating Type Switching ◽  
A Site

A CIS-ACTING MUTATION WITHIN THE MAT  a LOCUS OF SACCHAROMYCES CEREVISIAE THAT PREVENTS EFFICIENT HOMOTHALLIC MATING-TYPE SWITCHING

Genetics ◽  
1980 ◽  
Vol 94 (2) ◽  
pp. 341-360
Author(s):  
Deborah Wygal Mascioli ◽  
James E Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Pleiotropic Effect ◽  
Wild Type ◽  
Dominant Mutation ◽  
Cis Acting ◽  
Silent Genes ◽  
Factor Expression ◽  
Mating Type Switching ◽  
Ho Gene

ABSTRACT Homothallic strains of Saccharomyces cerevisiae are able to switch from one mating-type to the other as frequently as every cell division. We have identified a cis-dominant mutation of the MATa locus, designated MATa-inc, that can be converted to MATα at only about 5% of the normal efficiency. In homothallic MATa-inc/mata* diploids, the MATa-inc locus switched to MATα in only one of 30 cases, while the mata* locus switched to MATα in all 30 cases. The MATa-inc mutation can be "healed" by a series of switches, first to MATα and then to a normal allele of MATa. These data are consistent with the "cassette" model of HICKS, STRATHERN and HERSKOWITZ (1977), in which mating conversions involve the transposition of wild-type copies of a or α information from silent genes elsewhere in the genome. The MATa-inc mutation appears to alter a DNA sequence necessary for the replacement of MATa by MATα. The MATa-inc mutation has no other effect on MATa functions. In heterothallic backgrounds, the mutation has no effect on the sensitivity to α-factor, synthesis of a-factor, expression of barrier phenotype or ability to mate or sporulate.—The MATa-inc allele does, however, exhibit one pleiotropic effect. About 1% of homothallic MATa-inc cells become completely unable to switch mating type because ofmutations at HMa, the locus proposed to carry the silent copy of α information.—In addition, we have isolated a less efficient allele of the HO gene.

scholarly journals Mechanism of MAT alpha donor preference during mating-type switching of Saccharomyces cerevisiae.

1996 ◽  
Vol 16 (2) ◽  
pp. 657-668 ◽  
Author(s):  
X Wu ◽  
J K Moore ◽  
J E Haber
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Strand Break ◽  
Normal Donor ◽  
Alpha Cells ◽  
Cis Acting ◽  
Mating Type Switching ◽  
Chromosome Iii ◽  
The Right ◽  
Donor Preference

During homothallic switching of the mating-type (MAT) gene in Saccharomyces cerevisiae, a- or alpha-specific sequences are replaced by opposite mating-type sequences copied from one of two silent donor loci, HML alpha or HMRa. The two donors lie at opposite ends of chromosome III, approximately 190 and 90 kb, respectively, from MAT. MAT alpha cells preferentially recombine with HMR, while MATa cells select HML. The mechanisms of donor selection are different for the two mating types. MATa cells, deleted for the preferred HML gene, efficiently use HMR as a donor. However, in MAT alpha cells, HML is not an efficient donor when HMR is deleted; consequently, approximately one-third of HO HML alpha MAT alpha hmr delta cells die because they fail to repair the HO endonuclease-induced double-strand break at MAT. MAT alpha donor preference depends not on the sequence differences between HML and HMR or their surrounding regions but on their chromosomal locations. Cloned HMR donors placed at three other locations to the left of MAT, on either side of the centromere, all fail to act as efficient donors. When the donor is placed 37 kb to the left of MAT, its proximity overcomes normal donor preference, but this position is again inefficiently used when additional DNA is inserted in between the donor and MAT to increase the distance to 62 kb. Donors placed to the right of MAT are efficiently recruited, and in fact a donor situated 16 kb proximal to HMR is used in preference to HMR. The cis-acting chromosomal determinants of MAT alpha preference are not influenced by the chromosomal orientation of MAT or by sequences as far as 6 kb from HMR. These data argue that there is an alpha-specific mechanism to inhibit the use of donors to the left of MAT alpha, causing the cell to recombine most often with donors to the right of MAT alpha.

Sign in / Sign up

Export Citation Format

Share Document