scholarly journals Identification of a member of a DNA-dependent ATPase family that causes interference with silencing.

1997 ◽  
Vol 17 (9) ◽  
pp. 5461-5472 ◽  
Author(s):  
Z Zhang ◽  
A R Buchman
Keyword(s):  
Mating Type ◽  
Tandem Repeats ◽  
Specific Interaction ◽  
Cis Acting ◽  
Cellular Processes ◽  
Protein Dna Interactions ◽  
Mating Type Switching ◽  
Silencer Elements ◽  
Dna Template ◽  
Knockout Mutation

DNA in eukaryotic cells is packed in tandem repeats of nucleosomes or higher-order chromatin structures, which present obstacles to many cellular processes that require protein-DNA interactions, such as transcription, DNA repair, and recombination. To find proteins that are involved in increasing the accessibility of specific DNA regions in yeast, we used a genetic approach that exploited transcriptional silencing normally occurring at HML and HMR loci. The silencing is mediated by cis-acting silencer elements and is thought to require the formation of a special chromatin structure that prevents accessibility to the silenced DNA. A previously uncharacterized gene, termed DIS1, was isolated from a screen for genes that interfere with silencing when overexpressed. DIS1 encodes a protein with conserved motifs that are present in a family of DNA-dependent ATPases, the SWI2/SNF2-like proteins. Overproduction of N-terminal half of DIS1 protein interfered specifically with ectopic silencing used in the screen as well as HMR E silencing. Two-hybrid studies revealed a specific interaction between the N terminus of DIS1 and the C-terminal half of SIR4, a protein essential for silencing. Cells with a dis1 knockout mutation had significantly lower mating-type switching rate. These results suggest that DIS1 may contribute to making the silenced DNA template at HM loci more accessible during the mating-type switching process.

scholarly journals Specific repression of the yeast silent mating locus HMR by an adjacent telomere.

1994 ◽  
Vol 14 (1) ◽  
pp. 446-455 ◽  
Author(s):  
J S Thompson ◽  
L M Johnson ◽  
M Grunstein
Keyword(s):  
Mating Type ◽  
Chromosomal Location ◽  
Regulatory Genes ◽  
Histone H4 ◽  
Cis Acting ◽  
N Terminus ◽  
Silencer Elements ◽  
Chromosome Iii

The yeast silent mating loci HML and HMR are located at opposite ends of chromosome III adjacent to the telomeres. Mutations in the N terminus of histone H4 have been previously found to derepress the yeast silent mating locus HML to a much greater extent than HMR. Although differences in the a and alpha mating-type regulatory genes and in the cis-acting silencer elements do not appear to strongly influence the level of derepression at HMR, we have found that the differential between the two silent cassettes is largely due to the position of the HMR cassette relative to the telomere on chromosome III. While HML is derepressed to roughly the same extent by mutations in histone H4 regardless of its chromosomal location, HMR is affected to different extends depending upon its chromosomal positioning. We have found that HMR is more severely derepressed by histone H4 mutations when positioned far from the telomere (cdc14 locus on chromosome VI) but is only minimally affected by the same mutations when integrated immediately adjacent to another telomere (ADH4 locus on chromosome VII). These data indicate that the degree of silencing at HMR is regulated in part by its neighboring telomere over a distance of at least 23 kb and that this form of regulation is unique for HMR and not present at HML. These data also indicate that histone H4 plays an important role in regulating the silenced state at both HML and HMR.

scholarly journals Uneven Distribution of Mating Types among Genotypes of Candida glabrata Isolates from Clinical Samples

2009 ◽  
Vol 8 (3) ◽  
pp. 287-295 ◽  
Author(s):  
Sylvain Brisse ◽  
Christine Pannier ◽  
Adela Angoulvant ◽  
Thierry de Meeus ◽  
Laure Diancourt ◽  
...  
Keyword(s):  
Mating Type ◽  
Candida Glabrata ◽  
Tandem Repeats ◽  
Minimum Spanning Tree ◽  
Variable Number ◽  
Clinical Samples ◽  
Population Genetic Analysis ◽  
Pathogenic Yeast ◽  
Diploid Genotype ◽  
Mating Type Switching

ABSTRACT In order to shed light on its basic biology, we initiated a population genetic analysis of Candida glabrata, an emerging pathogenic yeast with no sexual stage yet recognized. A worldwide collection of clinical strains was subjected to analysis using variable number of tandem repeats (VNTR) at nine loci. The clustering of strains obtained with this method was congruent with that obtained using sequence polymorphism of the NMT1 gene, a locus previously proposed for lineage assignment. Linkage disequilibrium supported the hypothesis of a mainly clonal reproduction. No heterozygous diploid genotype was found. Minimum-spanning tree analysis of VNTR data revealed clonal expansions and associated genotypic diversification. Mating type analysis revealed that 80% of the strains examined are MAT a and 20% MATα and that the two alleles are not evenly distributed. The MAT a genotype dominated within large clonal groups that contained only one or a few MATα types. In contrast, two groups were dominated by MATα strains. Our data are consistent with rare independent mating type switching events occurring preferentially from type a to α, although the alternative possibility of selection favoring type a isolates cannot be excluded.

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.

Specific repression of the yeast silent mating locus HMR by an adjacent telomere

1994 ◽  
Vol 14 (1) ◽  
pp. 446-455
Author(s):  
J S Thompson ◽  
L M Johnson ◽  
M Grunstein
Keyword(s):  
Mating Type ◽  
Chromosomal Location ◽  
Regulatory Genes ◽  
Histone H4 ◽  
Cis Acting ◽  
N Terminus ◽  
Silencer Elements ◽  
Chromosome Iii

The yeast silent mating loci HML and HMR are located at opposite ends of chromosome III adjacent to the telomeres. Mutations in the N terminus of histone H4 have been previously found to derepress the yeast silent mating locus HML to a much greater extent than HMR. Although differences in the a and alpha mating-type regulatory genes and in the cis-acting silencer elements do not appear to strongly influence the level of derepression at HMR, we have found that the differential between the two silent cassettes is largely due to the position of the HMR cassette relative to the telomere on chromosome III. While HML is derepressed to roughly the same extent by mutations in histone H4 regardless of its chromosomal location, HMR is affected to different extends depending upon its chromosomal positioning. We have found that HMR is more severely derepressed by histone H4 mutations when positioned far from the telomere (cdc14 locus on chromosome VI) but is only minimally affected by the same mutations when integrated immediately adjacent to another telomere (ADH4 locus on chromosome VII). These data indicate that the degree of silencing at HMR is regulated in part by its neighboring telomere over a distance of at least 23 kb and that this form of regulation is unique for HMR and not present at HML. These data also indicate that histone H4 plays an important role in regulating the silenced state at both HML and HMR.

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