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RNA-seq and ChIP-seq of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

ABSTRACT: RNA-seq and ChIP-seq of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

PROVIDER: PRJNA503582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8146850.fastq.gz	Fastqsanger.gz
	SRR8146860.fastq.gz	Fastqsanger.gz
	SRR8146870.fastq.gz	Fastqsanger.gz
	SRR8146880.fastq.gz	Fastqsanger.gz
	SRR8146851.fastq.gz	Fastqsanger.gz

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RNA sequencing data of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

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.

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RNA sequencing data of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

Project description:RNA sequencing data of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

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Genome-wide occupanies of Ssu72, Pol II, pSer2, pSer5, pSer7 and pThr4 of Ssu72 Wild Type and Knock-out MEFs and hepatocytes

Project description:We report the genome-wide occupanies for high-throughput profiling of Pol II and Pol II CTD phosphorylation modifications in mammalian cells and tissues. By obtaining over three billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, embryonic fibroblasts and primary hepatocytes. Loss of mammalian Ssu72 was found to be related to defect of transcriptional elongation though the defects of Pol II CTD phophorylational dynamics. In addition, depletion of Ssu72 resulted in defects of Pol II elongation by reducing CTD Ser2 and Thr4 phosphorylation which induced Pol II accumulation at the proximal promoter region by increasing CTD Ser5 and Ser7 phosphorylation of transcriptionally active genes in a tissue-specific manner. Our results revealed a fundamental role of mammalian Ssu72 in regulating RNA Pol II-mediated transcriptional plasticity for cell-type-specific homeostatic maintenance.

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Genome-wide occupanies of Ssu72, Pol II, pSer2, pSer5, pSer7 and pThr4 of Ssu72 Wild Type and Knock-out MEFs and hepatocytes

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RNA-seq and ChIP-seq of Ssu72 Wild Type and Knock-Out MEFs, hepatocytes and ES cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression profile of MEFs, iPS, and ES in different culture condition

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RNA-seq analysis in ssu72 mutant cells [WT_ssu72]

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.

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