Fission yeast telomeres are packaged into a non-canonical histone-containing chromatin structure dependent on Shelterin and RNA.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA422399 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6376100_1.fastq.gz | Fastqsanger.gz | |||
| SRR6376100_2.fastq.gz | Fastqsanger.gz | |||
| SRR6376101_1.fastq.gz | Fastqsanger.gz | |||
| SRR6376101_2.fastq.gz | Fastqsanger.gz | |||
| SRR6376102_1.fastq.gz | Fastqsanger.gz |
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Project description:Yeast telomeres exist in a distinct protected structure at the chromsome end. This structure, termed the telosome, has long been thought to be free of histones. Here we show that this is not the case - telomere repeats are indeed associated with histones. This finding has implications for telomere function and ultrastructure.
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Project description:The localization of condensin along chromosomes is crucial for their accurate segregation in anaphase. Condensin is enriched at telomeres but how and for what purpose had remained elusive. Here we show that fission yeast condensin accumulates at telomere repeats through the balancing acts of Taz1, a core component of the shelterin complex that ensures telomeric functions, and Mit1, a nucleosome-remodeler associated with shelterin. We further show that condensin takes part in sister-telomere separation in anaphase, and that this event can be uncoupled from the prior separation of chromosomes arms, implying a telomere-specific separation mechanism. Consistent with a cis-acting process, increasing or decreasing condensin occupancy specifically at telomeres modifies accordingly the efficiency of their separation in anaphase. Genetic evidence suggests that condensin promotes sister-telomere separation by counteracting cohesin. Thus, our results reveal a shelterin-based mechanism that enriches condensin at telomeres to drive in cis their separation during mitosis.
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Project description:Occupancy profiling of Shelterin components in fission yeast. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation. Whole cell extract DNA and DNA recovered from Taz1 or Rif1-immunoprecipitated chromatin of fission yeast were random-prime PCR amplified and labeled with Cy3 (whole cell extract DNA) or with Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
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Project description:Occupancy profiling of Shelterin components in fission yeast. Facultative heterochromatin regulates gene expression, but its assembly is poorly understood. Previously, we identified facultative heterochromatin islands in the fission yeast genome and found that RNA elimination machinery promotes island assembly at meiotic genes. Here, we report that Taz1, a component of the telomere protection complex Shelterin, is required to assemble heterochromatin islands at regions corresponding to late replication origins that are sites of double-strand break formation during meiosis. The loss of Taz1 and other Shelterin subunits, including Ccq1 that interacts with Clr4/Suv39h, abolishes heterochromatin at late origins and causes defective silencing of associated genes. Moreover, the late origin regulator Rif1 affects heterochromatin at Taz1-dependent islands and subtelomeric regions. We uncover a connection between heterochromatin and replication control, and show that heterochromatin factors affect timing of replication. These analyses implicate Shelterin in facultative heterochromatin assembly at late origins, which has important implications for the maintenance of genome stability and gene regulation.
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Project description:The dynamic nature of genome organization impacts critical nuclear functions including the regulation of gene expression, replication and DNA damage repair. Despite significant progress, the mechanisms responsible for reorganization of the genome in response to cellular stress, such as aberrant DNA replication, are poorly understood. Here we show that fission yeast cells carrying a mutation in the DNA-binding protein Sap1 show defects in DNA replication progression and genome stability, and display extensive changes in genome organization. Chromosomal regions such as subtelomeres that show defects in replication progression associate with the nuclear envelope in sap1 mutant cells. Moreover, high-resolution Hi-C analysis revealed prominent new interactions between telomeres and chromosomal arm regions containing replication origins proximal to binding sites for Taz1, a component of the Shelterin telomere protection complex. Strikingly, we find that Shelterin components promote interactions between Taz1-associated chromosomal arm regions and telomeres. These analyses reveal an unexpected role for Shelterin in genome reorganization in cells experiencing replication stress, which has important implications for understanding mechanisms governing replication and genome stability.
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Project description:The dynamic nature of genome organization impacts critical nuclear functions including the regulation of gene expression, replication and DNA damage repair. Despite significant progress, the mechanisms responsible for reorganization of the genome in response to cellular stress, such as aberrant DNA replication, are poorly understood. Here we show that fission yeast cells carrying a mutation in the DNA-binding protein Sap1 show defects in DNA replication progression and genome stability, and display extensive changes in genome organization. Chromosomal regions such as subtelomeres that show defects in replication progression associate with the nuclear envelope in sap1 mutant cells. Moreover, high-resolution Hi-C analysis revealed prominent new interactions between telomeres and chromosomal arm regions containing replication origins proximal to binding sites for Taz1, a component of the Shelterin telomere protection complex. Strikingly, we find that Shelterin components promote interactions between Taz1-associated chromosomal arm regions and telomeres. These analyses reveal an unexpected role for Shelterin in genome reorganization in cells experiencing replication stress, which has important implications for understanding mechanisms governing replication and genome stability.
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Project description:The dynamic nature of genome organization impacts critical nuclear functions including the regulation of gene expression, replication and DNA damage repair. Despite significant progress, the mechanisms responsible for reorganization of the genome in response to cellular stress, such as aberrant DNA replication, are poorly understood. Here we show that fission yeast cells carrying a mutation in the DNA-binding protein Sap1 show defects in DNA replication progression and genome stability, and display extensive changes in genome organization. Chromosomal regions such as subtelomeres that show defects in replication progression associate with the nuclear envelope in sap1 mutant cells. Moreover, high-resolution Hi-C analysis revealed prominent new interactions between telomeres and chromosomal arm regions containing replication origins proximal to binding sites for Taz1, a component of the Shelterin telomere protection complex. Strikingly, we find that Shelterin components promote interactions between Taz1-associated chromosomal arm regions and telomeres. These analyses reveal an unexpected role for Shelterin in genome reorganization in cells experiencing replication stress, which has important implications for understanding mechanisms governing replication and genome stability.
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