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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

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

PROVIDER: PRJNA503584 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8146850.fastq.gz	Fastqsanger.gz
	SRR8146860.fastq.gz	Fastqsanger.gz
	SRR8146870.fastq.gz	Fastqsanger.gz
	SRR8146851.fastq.gz	Fastqsanger.gz
	SRR8146861.fastq.gz	Fastqsanger.gz

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

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Project description:Selective degradation of endoplasmic reticulum (ER) via autophagy receptors is important to maintain cell homeostasis. In this study we identify FAM134A/RETREG2 and FAM134C/RETREG3 as bona fide ER-phagy receptors containing a classical and functional LIR motif. In contrast to the other family member FAM134B/RETREG1, over-expressed FAM134A and C are in a relatively inactive state, under basal conditions, and require an activation signal to fragment significant amounts of ER. Global proteomes analysis of knockout MEFs suggests distinct and overlapping functions of the three FAM134. Common functions are the maintenance of the ER shape and delivery of mis-folded pro-collagen I to lysosomes. Single knockout of Fam134a or Fam134c lead to swollen ER and massive intracellular accumulation of pro-collagen I. In this context, Fam134a but not Fam134c over-expression is able to recover collagen I levels, in Fam134b knockout MEFs, indicating distinct modes of action. Moreover, we provide evidence that Fam134a has a LIR-independent function in maintaining collagen I homeostasis in a co-receptor complex together with Fam134c. This pathway works in parallel to Fam134b, which in contrast is self-sufficient to drive ER-phagy.

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

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