RNA-seq analysis in ssu72 mutant cells [WT_ssu72]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604125 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10994100_1.fastq.gz | Fastqsanger.gz | |||
| SRR10994100_2.fastq.gz | Fastqsanger.gz | |||
| SRR10994101_1.fastq.gz | Fastqsanger.gz | |||
| SRR10994101_2.fastq.gz | Fastqsanger.gz | |||
| SRR10994102_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:We report accumulation of cryptic antisense transcripts in ssu72 mutant cells. A histone deacetylase (Hos2) is not required to repress the cryptic transcription in SSU72+ strain however in ssu72 mutant cells, Hos2 has an important role in suppression of the cryptic transcription Phosphorylation of the RNA polymerase II C-terminal domain on heptad Y1S2P3T4S5P6S7 coordinates key events during transcription and when its deregulation leads to defects in transcription and RNA processing. Here we report that histone deacetylase complex activity of the fission yeast Hos2/Set3 complex plays an important role in suppressing cryptic initiation of the antisense transcription when the C-terminal domain phosphorylation is dysregulated due to the loss of Ssu72 phosphatase. Interestingly, while single hos2/set3 mutants have little effect, loss of hos2 or set3 in addition to ssu72? leads to synergistic increase in antisense transcription globally and correlates with increases genomic instability and formation of deleterious R-loop structures across these regions. We propose that Ssu72 is essential to suppress initiation of cryptic transcription in the 3?end of the RNA polymerase II transcribed regions. In the absence of Ssu72, antisense transcription is supressed by the Hos2/Set3 dependent surveillance mechanism to maintain genome stability.
2020-06-30 | GSE144591 | GEO
Project description:RNA-seq analysis in ssu72 and hos2 mutant cells
| PRJNA604124 | ENA
Project description:We report accumulation of cryptic antisense transcripts in ssu72 mutant cells. A histone deacetylase (Hos2) is not required to repress the cryptic transcription in SSU72+ strain however in ssu72 mutant cells, Hos2 has an important role in suppression of the cryptic transcription Phosphorylation of the RNA polymerase II C-terminal domain on heptad Y1S2P3T4S5P6S7 coordinates key events during transcription and when its deregulation leads to defects in transcription and RNA processing. Here we report that histone deacetylase complex activity of the fission yeast Hos2/Set3 complex plays an important role in suppressing cryptic initiation of the antisense transcription when the C-terminal domain phosphorylation is dysregulated due to the loss of Ssu72 phosphatase. Interestingly, while single hos2/set3 mutants have little effect, loss of hos2 or set3 in addition to ssu72? leads to synergistic increase in antisense transcription globally and correlates with increases genomic instability and formation of deleterious R-loop structures across these regions. We propose that Ssu72 is essential to suppress initiation of cryptic transcription in the 3?end of the RNA polymerase II transcribed regions. In the absence of Ssu72, antisense transcription is supressed by the Hos2/Set3 dependent surveillance mechanism to maintain genome stability.
2020-06-30 | GSE144592 | GEO
Project description:Deletion of ssu72 gene leads to a transcription elongation defect and the increase in the level of Ser5 and Ser7 phosphorylation in CTD of Rpb1 Phosphorylation of the RNA polymerase II C-terminal domain on heptad Y1S2P3T4S5P6S7 coordinates key events during transcription and when its deregulation leads to defects in transcription and RNA processing. Here we report that histone deacetylase complex activity of the fission yeast Hos2/Set3 complex plays an important role in suppressing cryptic initiation of the antisense transcription when the C-terminal domain phosphorylation is dysregulated due to the loss of Ssu72 phosphatase. Interestingly, while single hos2/set3 mutants have little effect, loss of hos2 or set3 in addition to ssu72? leads to synergistic increase in antisense transcription globally and correlates with increases genomic instability and formation of deleterious R-loop structures across these regions. We propose that Ssu72 is essential to suppress initiation of cryptic transcription in the 3?end of the RNA polymerase II transcribed regions. In the absence of Ssu72, antisense transcription is supressed by the Hos2/Set3 dependent surveillance mechanism to maintain genome stability.
2020-06-30 | GSE144594 | GEO
Project description:Deletion of ssu72 gene leads to a transcription elongation defect and the increase in the level of Ser5 and Ser7 phosphorylation in carboxy-terminal domain (CTD) of Rpb1 Phosphorylation of the RNA polymerase II C-terminal domain on heptad Y1S2P3T4S5P6S7 coordinates key events during transcription and when its deregulation leads to defects in transcription and RNA processing. Here we report that histone deacetylase complex activity of the fission yeast Hos2/Set3 complex plays an important role in suppressing cryptic initiation of the antisense transcription when the C-terminal domain phosphorylation is dysregulated due to the loss of Ssu72 phosphatase. Interestingly, while single hos2/set3 mutants have little effect, loss of hos2 or set3 in addition to ssu72? leads to synergistic increase in antisense transcription globally and correlates with increases genomic instability and formation of deleterious R-loop structures across these regions. We propose that Ssu72 is essential to suppress initiation of cryptic transcription in the 3?end of the RNA polymerase II transcribed regions. In the absence of Ssu72, antisense transcription is supressed by the Hos2/Set3 dependent surveillance mechanism to maintain genome stability.
2020-06-30 | GSE144593 | GEO
Project description:To investigate how mammalian Ssu72 regulated gene expression, we performed RNA-Seq analyses of Ssu72 in three different cell types depending on their proliferation capabilities: embryonic stem (ES) cells (highly proliferating), primary murine embryonic fibroblasts (MEFs) (moderate proliferating), and hepatocytes (almost quiescent). Ssu72 deletion was induced by infection with Cre recombinase adenovius (Ad-Cre). Infection of ESf/f, MEFf/f, and hepatocytef/f with Ad-Cre resulted in efficient reduction of Ssu72 levels. Depletion of Ssu72 resulted in downregulation or upregulation of large subsets of genes in three different cell types.
2020-12-28 | GSE122101 | GEO
Project description:Genome-wide maps of RNA polymerase II in WT and ssu72 mutant cells [S5_S7_ChIPseq]
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Project description:Genome-wide maps of RNA polymerase II in WT and ssu72 mutant cells [8WG16_S2_Y1_ChIPseq]
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Project description:RNA-Seq analysis carried out in three different backcrosses based on Iberian breed with Landrace, Pietrain and Duroc breeds
2017-10-31 | PRJEB23068 | EVA
Project description:Genome-wide analysis of ssu72 and rrp6 mutants in Yeast
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