Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA298343 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2601770_1.fastq.gz | Fastqsanger.gz | |||
| SRR2601770_2.fastq.gz | Fastqsanger.gz | |||
| SRR2601780_1.fastq.gz | Fastqsanger.gz | |||
| SRR2601780_2.fastq.gz | Fastqsanger.gz | |||
| SRR2601790_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Yeast chromosome III contains the mating type loci that provide a paradigm for long-range interactions between distant loci. Yeast switch mating type by gene conversion between the MAT locus and either of two silent loci (HML or HMR) on opposite ends of the chromosome. This long-range process is mating type-specific so that MATa cells choose HML as template, while MATα cells use HMR. The Recombination Enhancer (RE), located on the left arm regulates this process. One long-standing hypothesis is that switching is guided by mating type-specific, and possibly RE-dependent three-dimensional folding of chromosome III. Here we used Hi-C, 5C, and live cell imaging to characterize the conformation of chromosome III in both mating types in non-switching strains. We discovered a mating type-specific difference in the folding of the left arm: in MATa cells the left arm is located closely to the centromere-proximal portion of the chromosome as well as to MAT, whereas it is more extended away in MATα cells. Deletion analysis showed that a 1 kb subregion within the RE, which is not necessary during switching, abolished mating type-dependent chromosome folding. In this mutant the conformation of chromosome III is the same in both mating types, but distinct from the wild type MATa or MATα conformations, indicating that the RE induces conformational changes in both mating types. The RE is therefore a composite element with one subregion essential for selecting the appropriate donor during switching, and a separate region involved in modulating chromosome conformation prior to switching.
2015-11-20 | GSE73890 | GEO
Project description:Yeast chromosome III contains the mating type loci that provide a paradigm for long-range interactions between distant loci. Yeast switch mating type by gene conversion between the MAT locus and either of two silent loci (HML or HMR) on opposite ends of the chromosome. This long-range process is mating type-specific so that MATa cells choose HML as template, while MATα cells use HMR. The Recombination Enhancer (RE), located on the left arm regulates this process. One long-standing hypothesis is that switching is guided by mating type-specific, and possibly RE-dependent three-dimensional folding of chromosome III. Here we used Hi-C, 5C, and live cell imaging to characterize the conformation of chromosome III in both mating types in non-switching strains. We discovered a mating type-specific difference in the folding of the left arm: in MATa cells the left arm is located closely to the centromere-proximal portion of the chromosome as well as to MAT, whereas it is more extended away in MATα cells. Deletion analysis showed that a 1 kb subregion within the RE, which is not necessary during switching, abolished mating type-dependent chromosome folding. In this mutant the conformation of chromosome III is the same in both mating types, but distinct from the wild type MATa or MATα conformations, indicating that the RE induces conformational changes in both mating types. The RE is therefore a composite element with one subregion essential for selecting the appropriate donor during switching, and a separate region involved in modulating chromosome conformation prior to switching. This submission contain 2 biological replicates of Hi-C experiments done in MATa and MATalpha cells in Saccharamycese cerevisiae. It also contains 3 biological replicates of 13 5C experiments in various mutants in MATa and MATalpha cells.
2015-11-20 | E-GEOD-73890 | biostudies-arrayexpress
Project description:Regulation of yeast chromosome III architecture and mating-type switching by a Sir2/condensin-bound region of the recombination enhancer [HiC-Seq]
| PRJNA358415 | ENA
Project description:Regulation of yeast chromosome III architecture and mating-type switching by a Sir2/condensin-bound region of the recombination enhancer [ChIP-Seq]
| PRJNA358416 | ENA
Project description:Saccharomyces cerevisiae switches its mating type (MATa or MATalpha) through gene conversion using one of two possible donors, HMLalpha or HMRa, both of which are maintained by the SIR silencing complex as heterochromatic cassettes on opposing ends of chromosome III. In MATa cells, HMLalpha on the left arm is preferentially chosen as the donor through a mechanism requiring a cis-acting sequence called the recombination enhancer (RE). The left half of the RE is required for this donor preference activity, whereas the right half has been implicated in regulating chromosome III structure. In this study we have identified a MATa-specific Sir2 and condensin binding site within the right half of the RE that maintains chromosome III in a switching-competent conformation by preventing MATa from interacting with the default HMRa donor on the right arm. Within the RE, Sir2 strongly represses transcription of a small MATa-specific gene of unknown function (RDT1). Upon expression of HO endonuclease to induce the switching process, Sir2 redistributes from the RE to the double-stranded DNA break site at MATa, thus derepressing RDT1 transcription to coincide with the timing of mating-type switching. Condensin is also displaced from the RE in response to the HO-induced break, likely contributing to the transient change in chromosome III conformation required for effective switching without disruption of HML and HMR heterochromatin.
2019-05-23 | GSE92715 | GEO
Project description:Saccharomyces cerevisiae switches its mating type (MATa or MATalpha) through gene conversion using one of two possible donors, HMLalpha or HMRa, both of which are maintained by the SIR silencing complex as heterochromatic cassettes on opposing ends of chromosome III. In MATa cells, HMLalpha on the left arm is preferentially chosen as the donor through a mechanism requiring a cis-acting sequence called the recombination enhancer (RE). The left half of the RE is required for this donor preference activity, whereas the right half has been implicated in regulating chromosome III structure. In this study we have identified a MATa-specific Sir2 and condensin binding site within the right half of the RE that maintains chromosome III in a switching-competent conformation by preventing MATa from interacting with the default HMRa donor on the right arm. Within the RE, Sir2 strongly represses transcription of a small MATa-specific gene of unknown function (RDT1). Upon expression of HO endonuclease to induce the switching process, Sir2 redistributes from the RE to the double-stranded DNA break site at MATa, thus derepressing RDT1 transcription to coincide with the timing of mating-type switching. Condensin is also displaced from the RE in response to the HO-induced break, likely contributing to the transient change in chromosome III conformation required for effective switching without disruption of HML and HMR heterochromatin.
2019-05-23 | GSE92714 | GEO
Project description:We designed and synthesized synI, which is ~21.4% shorter than native chrI, the smallest chromosome in Saccharomyces cerevisiae. SynI was designed for attachment to another synthetic chromosome due to concerns surrounding potential instability and karyotype imbalance, and is now attached to synIII, yielding the first synthetic yeast fusion chromosome. We constructed additional fusion chromosomes to investigate effects of fusions on nuclear function. We observed unexpected loops and twisted structures in chrIII-I and chrIX-III-I fusion chromosomes dependent on silencing protein Sir3. ChrI faces special challenges in assuring meiotic crossovers required for efficient homolog disjunction. Centromere deletions engineered into fusion chromosomes revealed opposing effects of core centromeres and pericentromeres in modulating deposition of meiotic recombination protein Red1. These effects extended over >100kb, to disproportionally promote meiotic recombination of small chromosomes like chrI. These findings reveal the power of synthetic genomics to uncover new biology and deconvolute complex biological systems.
2023-09-15 | GSE242509 | GEO
Project description:Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.
2017-09-12 | GSE98435 | GEO
Project description:Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.
2017-09-12 | GSE98282 | GEO
Project description:Regulation of yeast chromosome III architecture and mating-type switching by a Sir2/condensin-bound region of the recombination enhancer
| PRJNA358414 | ENA