Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin
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ABSTRACT:
PROVIDER: PRJNA432194 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6652860.fastq.gz | Fastqsanger.gz | |||
| SRR6652870.fastq.gz | Fastqsanger.gz | |||
| SRR6652880.fastq.gz | Fastqsanger.gz | |||
| SRR6652890_1.fastq.gz | Fastqsanger.gz | |||
| SRR6652890_2.fastq.gz | Fastqsanger.gz |
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Project description:The circadian rhythm controls timed choreography of gene expression to maintain normal cell physiology and metabolism. The predominant regulatory mechanism of the circadian rhythm is a transcriptional negative feedback loop that facilitates, and is facilitated by, circadian-regulated facultative heterochromatin. The long-term consequence of disrupted diurnal rhythm, or mutations in core clock genes, cause accelerated aging and an increased incidence in age-related diseases. To understand chromatin dynamics underlying age-related changes to circadian transcription, we performed a combined RNA-seq and ChIP-seq at two diurnal time-points for three different age groups. Our analysis focused on uncovering relationships between long non-coding RNA (lncRNA) and age-related changes to heterochromatin. We determined that the core clock genes maintain rhythmic expression regardless of age, but circadian output, including numerous lncRNAs, changes dramatically with age. In addition, there is both diurnal and age-related changes in Histone H3 lysine 9 tri-methylation (H3K9me3) that correlate with the changes in gene expression. Collectively, the data suggest a model where age-related changes in diurnal gene expression occur, in part, due to age-related redistribution of rhythmic facultative heterochromatin. Alterations in heterochromatin appear to be mediated by changes in diurnal lncRNA expression creating an interlocked circadian-chromatin regulatory network that undergoes age-dependent metamorphosis.
2018-01-30 | GSE109855 | GEO
Project description:The circadian rhythm controls timed choreography of gene expression to maintain normal cell physiology and metabolism. The predominant regulatory mechanism of the circadian rhythm is a transcriptional negative feedback loop that facilitates, and is facilitated by, circadian-regulated facultative heterochromatin. The long-term consequence of disrupted diurnal rhythm, or mutations in core clock genes, cause accelerated aging and an increased incidence in age-related diseases. To understand chromatin dynamics underlying age-related changes to circadian transcription, we performed a combined RNA-seq and ChIP-seq at two diurnal time-points for three different age groups. Our analysis focused on uncovering relationships between long non-coding RNA (lncRNA) and age-related changes to heterochromatin. We determined that the core clock genes maintain rhythmic expression regardless of age, but circadian output, including numerous lncRNAs, changes dramatically with age. In addition, there is both diurnal and age-related changes in Histone H3 lysine 9 tri-methylation (H3K9me3) that correlate with the changes in gene expression. Collectively, the data suggest a model where age-related changes in diurnal gene expression occur, in part, due to age-related redistribution of rhythmic facultative heterochromatin. Alterations in heterochromatin appear to be mediated by changes in diurnal lncRNA expression creating an interlocked circadian-chromatin regulatory network that undergoes age-dependent metamorphosis.
2018-01-30 | GSE109854 | GEO
Project description:Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (ChIP-Seq data set)
| PRJNA432201 | ENA
Project description:Long non-coding RNAs have age-dependent diurnal expression that correlates with age-related changes in genome-wide facultative heterochromatin (RNA-Seq data set)
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Project description:It is important to accurately regulate the expression of genes involved in development and environmental response. In the fission yeast Schizosaccharomyces pombe, meiotic genes are tightly repressed during vegetative growth. Despite being embedded in heterochromatin these genes are transcribed and believed to be repressed primarily at the level of RNA. However, the mechanism of facultative heterochromatin formation and the interplay with transcription regulation is not understood. We show genome-wide that HDAC-dependent histone deacetylation is a major determinant in transcriptional silencing of facultative heterochromatin domains. Indeed, mutation of class I/II HDACs leads to increased transcription of meiotic genes and accumulation of their mRNAs. Mechanistic dissection of the pho1 gene where, in response to phosphate, transient facultative heterochromatin is established by overlapping lncRNA transcription shows that the Clr3 HDAC contributes to silencing independently of SHREC, but in an lncRNA-dependent manner. We propose that HDACs promote facultative heterochromatin by establishing alternative transcriptional silencing.
2018-03-19 | GSE108668 | GEO
Project description:Occupancy profiling of Rec12 during fission yeast meiosis. 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 by Rec12 ChIP from fission yeast undergoing synchronous meiosis were random-prime PCR amplified and labeled with Cy3 (whole cell extract) or Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
2016-06-09 | E-GEOD-78821 | biostudies-arrayexpress
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.
2016-06-09 | E-GEOD-78822 | biostudies-arrayexpress
Project description:ChIP-chip analyses of lysine 9 dimethylated histone H3 in Shelterin mutants. 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 H3K9 dimethylated chromatin of fission yeast were random-prime PCR amplified and labeled with Cy3 (whole cell extract) or Cy5 (IP DNA) and analyzed using custom 60mer Agilent array that tiles Schizosaccharomyces pombe genome in 300bp intervals alternately on both strands.
2016-06-09 | E-GEOD-78820 | biostudies-arrayexpress
Project description:Facultative heterochromatin in the filamentous fungus Neurospora crassa is identified by the repressive histone mark H3K27me3 and is primarily subtelomeric, while constitutive heterochromatin, marked by the DIM-5-catalzyed H3K9me3, is found at centromeres, telomeres, and smaller dispersed regions. In strains lacking constitutive heterochromatin (e.g., Δdim-5), H3K27me2/3 relocalizes to the regions formerly marked by H3K9me3. H3K27me3 is catalyzed by the SET-7 histone methyltransferase subunit of the Polycomb Repressive Complex 2 (PRC2); another PRC2 member, Neurospora p55 (NPF) regulates subtelomeric H3K27me2/3. Despite the de-repression of >70 genes, a Δset-7 strain has no distinguishable phenotype. To investigate the facultative heterochromatin contribution to genome organization, we performed high-throughput “chromosome conformation capture” (Hi-C) on mutants with impacted H3K27me2/3 deposition. A Δset-7 strain has decreased inter-/intra-subtelomeric contacts among others; this pattern is mirrored in a Δnpf strain, which lacks subtelomeric H3K27me3. In a Δset-7 strain, telomere bundles were often uncoupled from the nuclear membrane and de-repressed genes were subtelomeric. The chromosome conformation of a Δset-7;Δdim-5 double mutant was similar to Δset-7, suggesting that facultative heterochromatin relocalization does not compensate for H3K9me3 loss and rescue the Neurospora genome organization in strains with defective constitutive heterochromatin.
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Project description:BrdU profiling of replication activity in hydroxyurea treated synchronous culture of 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. Cdc25-22 cells carrying thymidine kinase and human nucleoside transporter expression modules were arrested at the G2/M boundary. After release into the cell cycle in minimal medium supplemented with hydroxyurea and 5â-bromo-2â-deoxyuridine (BrdU) cells were collected at time corresponding to maximal septation index and fixed by treatment with sodium azide. BrdU labeled DNA was recovered by immunoprecipitation, amplified by random-primed PCR and after conjugation with Cy5 (IP) or Cy3 (input DNA) analyzed on Agilent 60mer array.
2016-06-09 | E-GEOD-78819 | biostudies-arrayexpress