Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA344330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4293181_1.fastq.gz | Fastqsanger.gz | |||
| SRR4293181_2.fastq.gz | Fastqsanger.gz | |||
| SRR4293182_1.fastq.gz | Fastqsanger.gz | |||
| SRR4293182_2.fastq.gz | Fastqsanger.gz | |||
| SRR4293183.fastq.gz | Fastqsanger.gz |
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Project description:KSRP knock-down and BMP2 treatment produce a largely overlapping reshape of the transcriptome in C2C12 cells. microRNAs (miRNAs) are essential regulators of development, physiology, and evolution with miRNA biogenesis being strictly controlled at multiple levels. Regulatory proteins, such as KH-type splicing regulatory protein (KSRP), modulate rates and timing of the enzymatic reactions responsible for maturation of select miRNAs from their primary transcripts in response to specific stimuli. Induction of myogenic miRNAs (myomiRs) is essential for muscle differentiation with KSRP phosphorylation being required to convey myogenic signals to enhanced myomiR maturation. Here we show that either KSRP silencing or Bone Morphogenetic Protein (BMP)2-signaling activation in mesenchimal C2C12 cells prevented myogenic differentiation while induced osteoblastic differentiation as revealed by the reshaping of the whole transcriptome analyzed by RNA deep-sequencing. The most striking feature common to both BMP2 signaling activation and KSRP silencing was a blockade of myomiR maturation. Our results demonstrate that phosphorylated SMAD proteins, the transducers of BMP signaling, associate with KSRP and block its interaction with primary-myomiRs. This, in turn, abrogates KSRP-dependent myomiR maturation with the knock-down of SMAD4, 5, and 9 being able to rescue KSRP function. SMAD-induced blockade of KSRP-dependent myomiR maturation, in parallel to the well known SMAD function on gene transcription, inhibits C2C12 cell differentiation into myofibers and contributes to orient cells towards osteoblast lineage. We propose that remodeling of co-regulatory complexes affecting primary-miRNA processing is a mechanism well suited to guide cell fate determination in eukaryotes. Total RNA was prepared from 1. untreated mock-transfected C2C12 cells; 2. BMP2-treated mock-transfected C2C12 cells; 3. untreated shKSRP-transfected C2C12 cells and analyzed by RNA-seq
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Project description:KSRP knock-down and BMP2 treatment produce a largely overlapping reshape of the transcriptome in C2C12 cells. microRNAs (miRNAs) are essential regulators of development, physiology, and evolution with miRNA biogenesis being strictly controlled at multiple levels. Regulatory proteins, such as KH-type splicing regulatory protein (KSRP), modulate rates and timing of the enzymatic reactions responsible for maturation of select miRNAs from their primary transcripts in response to specific stimuli. Induction of myogenic miRNAs (myomiRs) is essential for muscle differentiation with KSRP phosphorylation being required to convey myogenic signals to enhanced myomiR maturation. Here we show that either KSRP silencing or Bone Morphogenetic Protein (BMP)2-signaling activation in mesenchimal C2C12 cells prevented myogenic differentiation while induced osteoblastic differentiation as revealed by the reshaping of the whole transcriptome analyzed by RNA deep-sequencing. The most striking feature common to both BMP2 signaling activation and KSRP silencing was a blockade of myomiR maturation. Our results demonstrate that phosphorylated SMAD proteins, the transducers of BMP signaling, associate with KSRP and block its interaction with primary-myomiRs. This, in turn, abrogates KSRP-dependent myomiR maturation with the knock-down of SMAD4, 5, and 9 being able to rescue KSRP function. SMAD-induced blockade of KSRP-dependent myomiR maturation, in parallel to the well known SMAD function on gene transcription, inhibits C2C12 cell differentiation into myofibers and contributes to orient cells towards osteoblast lineage. We propose that remodeling of co-regulatory complexes affecting primary-miRNA processing is a mechanism well suited to guide cell fate determination in eukaryotes.
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Project description:RNA splicing is an essential step for expression of genes commonly altered in multiple liver diseases. However, how the spliceosomal components participate in the pathogenesis of acute liver failure (ALF) remains poorly defined. Here, we report that KH-type splicing regulatory protein (KSRP) which is downregulated in ALF, regulates RNA splicing in the liver through interacting with the Splicing factor 3b subunit 1 (SF3B1). Overexpression of KSRP resulted in marked amelioration of hepatic injury in vivo. Transcriptomic analysis reveals that KSRP depletion led to severe splicing defects in genes with significant intron retention. Such defects cause substantial loss of proliferation and apoptosis related genes such as EGFR, which further exaggerated liver injury. KSRP promotes RNA splicing of splicing related genes, including SF3B1, PHF5A, and SF3B4, indicating the existence of a positive feedback loop that regulates RNA splicing. Mechanistically, KSRP directly interacts with SF3B1 and enhances binding of SF3B1 to the branch sites located upstream of the exon. Overall, our findings demonstrate a novel mechanism by which KSPR protects against acute liver injury by promoting RNA splicing through interacting with the SF3B complex.
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