Ontology highlight
ABSTRACT:
PROVIDER: PRJNA278406 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1916780.fastq.gz | Fastqsanger.gz | |||
| SRR1916790.fastq.gz | Fastqsanger.gz | |||
| SRR1916771.fastq.gz | Fastqsanger.gz | |||
| SRR1916781.fastq.gz | Fastqsanger.gz | |||
| SRR1916772.fastq.gz | Fastqsanger.gz |
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Project description:Paf1 complex factors, Leo1 and Paf1, promote local histone turnover to modulate chromatin states in fission yeast [ncRNA-Seq]
| PRJNA278408 | ENA
Project description:Paf1 complex factors, Leo1 and Paf1, promote local histone turnover to modulate chromatin states in fission yeast [ChIP-exo]
| PRJNA278409 | ENA
Project description:Maintenance of open and repressed chromatin states is crucial for regulation of gene expression. To study the genes involved in maintaining chromatin states we generated a random mutant library using the Hermes transposon mutagenesis system in fission yeast Schizosacchromyces pombe. The silencing of reporter genes inserted in the euchromatic region adjacent to the heterochromatic mating type locus was monitored. We identified Leo1-Paf1, a subcomplex of the RNA Polymerase II Associated Factor 1 Complex (Paf1C), required to prevent spreading of heterochromatin into euchromatin. Through high-resolution genome-wide ChIP (ChIP-exo) we mapped the heterochromatin mark H3K9me2 in leo1∆ cells. Loss of Leo1-Paf1 led to increased heterochromatin stability at several facultative heterochromatin loci. The RNAi machinery is the major pathway for heterochromatin formation in S. pombe. However, small RNA sequencing showed that heterochromatin assembly in leo1∆ cells was RNAi-independent. By examining histone turnover rate in leo1∆ cells, we showed that deletion of Leo1 decreased nucleosome turnover, which led to heterochromatin spreading. Our data revealed that Leo1-Paf1 promotes chromatin state fluctuations by enhancing histone turnover.
2015-10-18 | GSE66940 | GEO
Project description:Maintenance of open and repressed chromatin states is crucial for regulation of gene expression. To study the genes involved in maintaining chromatin states we generated a random mutant library using the Hermes transposon mutagenesis system in fission yeast Schizosacchromyces pombe. The silencing of reporter genes inserted in the euchromatic region adjacent to the heterochromatic mating type locus was monitored. We identified Leo1-Paf1, a subcomplex of the RNA Polymerase II Associated Factor 1 Complex (Paf1C), required to prevent spreading of heterochromatin into euchromatin. Through high-resolution genome-wide ChIP (ChIP-exo) we mapped the heterochromatin mark H3K9me2 in leo1∆ cells. Loss of Leo1-Paf1 led to increased heterochromatin stability at several facultative heterochromatin loci. The RNAi machinery is the major pathway for heterochromatin formation in S. pombe. However, small RNA sequencing showed that heterochromatin assembly in leo1∆ cells was RNAi-independent. By examining histone turnover rate in leo1∆ cells, we showed that deletion of Leo1 decreased nucleosome turnover, which led to heterochromatin spreading. Our data revealed that Leo1-Paf1 promotes chromatin state fluctuations by enhancing histone turnover.
2015-10-18 | GSE66939 | GEO
Project description:Cellular quiescence is a reversible differentiation state when cells are changing the gene expression programme to reduce metabolic functions and adapt to a new cellular environment. The epigenetic changes that accompany these alterations are not so well understood. Here we investigate the role of Leo1, a subunit of the conserved Paf1 (RNA polymerase-associated factor 1) complex, in the quiescence process using fission yeast as a model organism. Fission yeast cells enter the G0 phase of the cell cycle when exposed to nitrogen starvation and the heterochromatin regions become very dynamic. The reduction of heterochromatin in early G0 correlates with the reduced activity of target of rapamycin, TORC2, signalling. Cells lacking the Leo1 show reduced survival in G0. In these cells heterochromatin regions including subtelomeres are stabilized and many genes, including membrane transport genes, fail to be expressed. Our results suggest that Leo1 is essential for dynamic regulation of heterochromatin and gene expression during cellular quiescence.
2019-06-30 | GSE116657 | GEO
Project description:Cellular quiescence is a reversible differentiation state when cells are changing the gene expression programme to reduce metabolic functions and adapt to a new cellular environment. The epigenetic changes that accompany these alterations are not so well understood. Here we investigate the role of Leo1, a subunit of the conserved Paf1 (RNA polymerase-associated factor 1) complex, in the quiescence process using fission yeast as a model organism. Fission yeast cells enter the G0 phase of the cell cycle when exposed to nitrogen starvation and the heterochromatin regions become very dynamic. The reduction of heterochromatin in early G0 correlates with the reduced activity of target of rapamycin, TORC2, signalling. Cells lacking the Leo1 show reduced survival in G0. In these cells heterochromatin regions including subtelomeres are stabilized and many genes, including membrane transport genes, fail to be expressed. Our results suggest that Leo1 is essential for dynamic regulation of heterochromatin and gene expression during cellular quiescence.
2019-06-30 | GSE116038 | GEO
Project description:Phf5a regulates occupancy of Paf1 complex in mouse myotubes. In this study we assayed for genome-wide localization of Leo1 subunit of the Paf1 complex in mouse myoblasts or myotubes under conditions of shControl or shPhf5a knockdown. These results revealed that downregualtion of Phf5a results in significant decrease of Leo1 binding to its targets in myotubes.
2016-08-31 | GSE86249 | GEO
Project description:Domains of heterochromatin play important roles in the maintenance and regulation of eukaryotic genomes. However, the repressive nature of heterochromatin combined with its propensity to self-propagate necessitates the existence of robust mechanisms that limit heterochromatin spreading and thereby avoid silencing of expressed genes. A number of specific sequence elements have been found to serve as barriers to heterochromatin spreading; however, the mechanisms by which spreading is curtailed are generally not well understood. Here we uncover a role for PAF complex component Leo1 in regulating heterochromatin cis-spreading. A genetic screen revealed that loss of Leo1 results in spreading of heterochromatin across a centromeric (IRC) boundary element in fission yeast. Similar heterochromatin spreading was seen upon deletion of other components of the PAF complex, but not other factors involved in transcription-coupled chromatin modification, indicating a specific role for the PAF complex in heterochromatin regulation. Loss of Leo1 is associated with reduced levels of H4K16 acetylation at the boundary, while tethering of the H4K16 acetyltransferase Mst1 to boundary chromatin suppresses heterochromatin spreading in leo1? cells, suggesting that Leo1 antagonises heterochromatin spreading by facilitating H4K16 acetylation. Interestingly, Leo1 also regulates heterochromatin spreading independently of boundaries, and loss of Leo1 causes redistribution of heterochromatin, in particular resulting in substantial expansion of telomeric heterochromatin domains. The PAF complex is known to be an important regulator of transcription-related chromatin modifications; our findings reveal a previously undescribed role for this complex in global regulation of heterochromatin spreading in cis. 8 samples: input (whole cell extract) and IP from H3K9me2 ChIP in wild-type and leo1? cells, in duplicate
2015-05-22 | E-GEOD-61688 | biostudies-arrayexpress
Project description:Phf5a regulates transcription elongation in mouse embryonic stem cells (ESCs), through regulation of the Paf1 complex. In this study we assayed for genome-wide localization of Paf1, Leo1 and Cdc73 subunits of the Paf1 complex in mouse ESCs under conditions of shControl and shPhf5a knockdown. These results revealed that downregualtion of Phf5a results in the significant decrease of Paf1 complex binding to its targets in ESCs.
2016-08-31 | GSE73445 | GEO
Project description:Release of promoter-proximal paused RNA polymerase II (Pol II) during early elongation is a critical step in transcriptional regulation in metazoan cells. Paused Pol II release is thought to require the kinase activity of cyclin-dependent kinase 9 (CDK9) for the phosphorylation of DRB sensitivity-inducing factor, negative elongation factor, and C-terminal domain (CTD) serine-2 of Pol II. We found that Pol II-associated factor 1 (PAF1) is a critical regulator of paused Pol II release, that positive transcription elongation factor b (P-TEFb) directly regulates the initial recruitment of PAF1 complex (PAF1C) to genes, and that the subsequent recruitment of CDK12 is dependent on PAF1C. These findings reveal cooperativity among P-TEFb, PAF1C, and CDK12 in pausing release and Pol II CTD phosphorylation. Comparison of the chromatin occupancy of [1] PAF1, CDC73, LEO1, CTR9, total Pol II, and CTD serine 2-phosphorylated Pol II by ChIP-seq in THP1 cells; [2] PAF1, Pol II, Pol II (ser-5p), CDK12, and CDK9 by ChIP-seq in control and PAF1 knockdown cells; [3] LEO1 and Pol II by ChIP-seq in control and flavopiridol treated THP1 cells.
2015-12-11 | E-GEOD-62171 | biostudies-arrayexpress