Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA358416 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5124300.fastq.gz | Fastqsanger.gz | |||
| SRR5124301.fastq.gz | Fastqsanger.gz | |||
| SRR5124302.fastq.gz | Fastqsanger.gz | |||
| SRR5124303.fastq.gz | Fastqsanger.gz | |||
| SRR5124304.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Regulation of yeast chromosome III architecture and mating-type switching by a Sir2/condensin-bound region of the recombination enhancer
| PRJNA358414 | 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: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:Purpose: This study was designed to determine the mechanism of condensin and Sir2 recruitment to the RDT1 promoter region of S. cerevisiae chromosome III, and to test whether preventing condensin recruitment by deleting the key factors, Fob1 and Lrs4, significantly alters the conformation of chromosome III. Conclusions: Conformational changes in chromosome III and loss of CEN12-rDNA looping in chromosome XII observed in lrs4? and fob1? mutants.
2023-03-23 | GSE198148 | 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.
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:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation. Genome-wide distributions of condensin and Pol III factors in fission yeast.
2015-08-12 | E-GEOD-60273 | biostudies-arrayexpress
Project description:purpose: investigation the global insights into Sir2-dependent gene silencing on all silent chromatin regions in budding yeast Method: RNA-sequencing Results: the Sir2 binding domain length caused by Sir2 spreading from the chromosomal end is different in each telomere in budding yeast. Expression of most subtelomeric genes increased in the ∆sir2 strain. Some Sir2-regulated subtelomeric genes were positioned within the telomeric Sir2-binding domain, while the others were outside the Sir2-binding domain. In addition, Sir2 was bound to the mating-type loci and rDNA region, and gene expression increased in the ∆sir2 strain. Conclusion: that S. cerevisiae has two modes of Sir2-mediated gene silencing: One is dependent on chromatin binding and spreading of Sir2, and the other is independent of spreading of Sir2
2021-12-16 | GSE190545 | GEO
Project description:Genome/chromosome organization is highly ordered and controls nuclear events. Here, we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensin to mediate interphase and mitotic chromosome organization in fission yeast. TBP recruits condensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; condensin in turn associates these genes with centromeres. Inhibition of the Cnd2-TBP interaction disrupts condensin localization across the genome and the proper assembly of mitotic chromosomes, leading to severe defects in chromosome segregation and eventually causing cellular lethality. We propose that the Cnd2-TBP interaction coordinates transcription with chromosomal architecture by linking dispersed gene loci with centromeres. This chromosome arrangement can contribute to the efficient transmission of physical force at the kinetochore to chromosomal arms, thereby supporting the fidelity of chromosome segregation.
2015-08-12 | GSE60273 | GEO