Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA278684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1917372_1.fastq.gz | Fastqsanger.gz | |||
| SRR1917372_2.fastq.gz | Fastqsanger.gz | |||
| SRR1917373_1.fastq.gz | Fastqsanger.gz | |||
| SRR1917373_2.fastq.gz | Fastqsanger.gz | |||
| SRR1917374_1.fastq.gz | Fastqsanger.gz |
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Project description:Alternative splicing greatly expands the proteomic diversity but its functional impact is often unclear. Here, we identify a highly conserved and temporally coordinated cell-type-specific splicing program, which is activated in part by ESRP2 during postnatal liver development. Consistent with failure of many neonatal-to-adult splicing transitions, Esrp2 null mice exhibit persistent expression of fetal markers and loss of mature hepatocyte characteristics. Conversely, ectopic expression of ESRP2 in immature mouse or human hepatocytes results in a reciprocal switch in splicing. Our findings define an essential role for ESRP2 in generation of conserved repertoires of adult splice isoforms that facilitate postnatal liver maturation. Mouse liver RNA was isolated with Trizol (Invitrogen). Hi-Seq libraries were prepared and paired-end 100bp Illumina sequencing was performed on mouse liver samples from different developmental stages.
2015-11-04 | E-GEOD-67009 | biostudies-arrayexpress
Project description:Alternative splicing greatly expands the proteomic diversity but its functional impact is often unclear. Here, we identify a highly conserved and temporally coordinated cell-type-specific splicing program, which is activated in part by ESRP2 during postnatal liver development. Consistent with failure of many neonatal-to-adult splicing transitions, Esrp2 null mice exhibit persistent expression of fetal markers and loss of mature hepatocyte characteristics. Conversely, ectopic expression of ESRP2 in immature mouse or human hepatocytes results in a reciprocal switch in splicing. Our findings define an essential role for ESRP2 in generation of conserved repertoires of adult splice isoforms that facilitate postnatal liver maturation.
2015-11-04 | GSE67009 | GEO
Project description:Postnatal period of development is critical for mammalian tissues and is coordinated through precise activation of genetic programs that govern differentiation, growth and maturation. Here, we describe a cell type- and developmental stage-specific program of alternative splicing that drives sequential replacement of fetal-to-adult protein isoforms in the mouse liver. Using deep transcriptome analysis of loss- & gain-of-function models we identified Epithelial Splicing regulatory protein 2 (ESRP2) as the major regulator for these developmental splicing decisions. Targeted deletion of ESRP2 in mice resulted in the failure of fetal-to-adult switch in splicing for hundreds of RNA transcripts that encode proteins involved in functional competence of hepatocytes. To delineate its role in activation of adult splicing program, we generated transgenic mice with tetracycline-inducible and hepatocyte-specific expression of ESRP2. Remarkably, premature expression of ESRP2 in the livers of newborn pups forced an earlier-than-normal onset of adult splicing program. To determine the in vivo ESRP2 RNA binding landscape within hepatocytes, we used CRISPR-Cas9 technology to FLAG-tag the endogenous locus of ESRP2 in mice and performed FLAG-eCLIP to identify genomewide binding sites. We identified ESRP2 as a regulator of miR-122 levels in hepatocytes, wherein this axis balances the polyploidization and proliferation states in postnatal hepatocytes.
2024-11-05 | GSE217391 | GEO
Project description:During liver regeneration, most new hepatocytes arise from pre-existing ones; yet, the underlying mechanisms that drive these cells from quiescence to proliferation remain poorly defined. By using high-resolution transcriptome profiling of polysome fractions from purified hepatocytes isolated from quiescent and toxin-injured adult mouse livers,we uncover the mRNA transcripts regulated during liver regeneration. The translational remodeling modulates protein levels of a set of splicing factors including Epithelial splicing regulatory protein 2 (ESRP2), which activates an early postnatal splicing program in regenerating hepatocytes as well as metabolic genes.
2018-09-17 | GSE106140 | GEO
Project description:During liver regeneration, most new hepatocytes arise from pre-existing ones; yet, the underlying mechanisms that drive these cells from quiescence to proliferation remain poorly defined. By using high-resolution transcriptome profiling of purified hepatocytes isolated from quiescent and toxin-injured adult mouse livers,we uncover an overlap of regenerative response with developmental transcriptome programming. The translational remodeling modulates protein levels ofa set of splicing factors including Epithelial splicing regulatory protein 2 (ESRP2), which activates an early postnatal splicing program in regenerating hepatocytes. We find that regeneration-regulated exons are enriched within unstructured regions of proteins and frequently harbor amino-acid residues that can be post-translationally modified to influence protein-protein interactions.
2018-09-17 | GSE105944 | GEO
Project description:Tumor-specific alternative splicing is implicated in the progression of cancer, including clear cell renal cell carcinoma (ccRCC). Using ccRCC RNA-sequencing data from The Cancer Genome Atlas, we found that epithelial splicing regulatory protein 2 (ESRP2), one of the key regulators of alternative splicing in epithelial cells, is expressed in ccRCC. ESRP2 mRNA expression did not correlate with the overall survival rate of ccRCC patients, but the expression of some ESRP-target exons correlated with the good prognosis and with the expression of Arkadia (also known as RNF111) in ccRCC. Arkadia physically interacted with ESRP2, induced polyubiquitination, and modulated its splicing function. Arkadia and ESRP2 suppressed ccRCC tumor growth in a coordinated manner. Lower expression of Arkadia correlated with advanced tumor stages and poor outcomes in ccRCC patients. This study thus reveals a novel tumor-suppressive role of the Arkadia-ESRP2 axis in ccRCC. Expression of mRNA in a ccRCC cell line OS-RC-2 under the knockdown of Arkadia or ESRP2. Knock-down of ESRP2 was confirmed by RT-PCR because of low expression of ESRP2 which resulted in non-quantitative FPKM value.
2015-08-01 | E-GEOD-66741 | biostudies-arrayexpress
Project description:ESRP2-miR122 axis regulates postnatal onset of polyploidization
| PRJNA898791 | ENA
Project description:Tissue- and cell-type specific regulators of alternative splicing (AS) are an essential layer of posttranscriptional gene regulation necessary for normal cellular function, patterning, and development. Here we report the Epithelial splicing regulatory proteins (Esrps) are required for patterning of multiple organs, with loss of both paralogs, Esrp1 and Esrp2, resulting in increasingly severe phenotypes. Global profiling of the Esrp splicing regulatory network from total epidermis revealed varied splicing sensitivity of Esrp targets upon loss of Esrp1 or double knockout. This may explain the progressive phenotypes seen in Esrp knockout mice, and these mice provide a unique genetic tool to evaluate functional consequences of epithelial splicing events in vivo. RNA from purified total epidermis (basal keratinocyte layer to cornified layer) of E18.5 mouse embryos were harvested by Trizol extraction. (Esrp1+/+, Esrp2-/- (n=2), Esrp1-/-, Esrp2+/+ (n=3), Esrp1-/-, Esrp2+/- (n=2), and Esrp1-/-, Esrp2-/- (n=2). 1 ug of total RNA was used for for RNA-seq library preparation using the TruSeq™ Stranded mRNA LT Sample Prep Kit (Illumina). 100x2 bp paired-end RNA-seq reads were generated on a HiSeq 2000 sequencer.
2015-09-08 | E-GEOD-64357 | biostudies-arrayexpress
Project description:Alternative splicing (AS) plays a critical role in cell fate transitions, development and disease. Recent studies have shown that AS also influences pluripotency and somatic cell reprogramming. We profiled transcriptome-wide AS changes that occur during reprogramming of fibroblasts to pluripotency. This analysis revealed distinct phases of AS during reprogramming, including a splicing program that is unique to transgene-independent iPS cells. Changes in the expression of alternative splicing factors Zcchc24, Esrp1, Mbnl1/2 and Rbm47 were demonstrated to be key contributors to phase-specific AS. RNA binding motif enrichment analysis near alternatively spliced exons provided further insight into the combinatorial regulation of AS during reprogramming by different RNA binding proteins. Ectopic expression of Esrp1 enhanced reprogramming, in part by modulating the AS of the epithelial specific transcription factor Grhl1.These data represent a comprehensive temporal analysis of the dynamic regulation of AS during the acquisition of pluripotency. ES cells from 3 independent E3.5 blastocysts from either Control (Esrp1 WT/WT; Esrp2 -/-) or Esrp DKO (Esrp1 floxed/floxed; Esrp2 -/-) were transfected with pLVX-EGFP-Cre, puro selected and RNA was isolated 6 days later.
2016-03-15 | E-GEOD-76222 | biostudies-arrayexpress
Project description:Tumor-specific alternative splicing is implicated in the progression of cancer, including clear cell renal cell carcinoma (ccRCC). Using ccRCC RNA-sequencing data from The Cancer Genome Atlas, we found that epithelial splicing regulatory protein 2 (ESRP2), one of the key regulators of alternative splicing in epithelial cells, is expressed in ccRCC. ESRP2 mRNA expression did not correlate with the overall survival rate of ccRCC patients, but the expression of some ESRP-target exons correlated with the good prognosis and with the expression of Arkadia (also known as RNF111) in ccRCC. Arkadia physically interacted with ESRP2, induced polyubiquitination, and modulated its splicing function. Arkadia and ESRP2 suppressed ccRCC tumor growth in a coordinated manner. Lower expression of Arkadia correlated with advanced tumor stages and poor outcomes in ccRCC patients. This study thus reveals a novel tumor-suppressive role of the Arkadia-ESRP2 axis in ccRCC.
2015-08-01 | GSE66741 | GEO