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Gene expression and splicing regulation by hnRNPU in skeletal muscle

ABSTRACT: Gene expression and splicing regulation by hnRNPU in skeletal muscle

PROVIDER: PRJNA607983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11140726_1.fastq.gz	Fastqsanger.gz
	SRR11140726_2.fastq.gz	Fastqsanger.gz
	SRR11140727_1.fastq.gz	Fastqsanger.gz
	SRR11140727_2.fastq.gz	Fastqsanger.gz
	SRR11140728_1.fastq.gz	Fastqsanger.gz

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Gene expression and splicing regulation by hnRNPU in skeletal muscle

Project description:Hnrnpu is the largest member of the heterogenous nuclear ribonucleoprotein family of RNA binding proteins. Hnrnpu is involved in pre-mRNA alternative splicing regulation. We used high throughput sequencing to determine how Hnrnpu regulates skeletal muscle physiology.

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microRNA-222 regulates muscle alternative splicing through Rbm24 during differentiation of skeletal muscle cells

Project description:A number of microRNAs have been shown to regulate skeletal muscle development and differentiation. MicroRNA-222 is downregulated during myogenic differentiation and its overexpression leads to alteration of muscle differentiation process and specialized structures. By using RNA induced silencing complex (RISC) pulldown followed by RNA sequencing, combined with in silico microRNA target prediction, we have identified two new targets of microRNA-222 involved in the regulation of myogenic differentiation, Ahnak and Rbm24. Specifically, the RNA binding protein Rbm24 is a major regulator of muscle specific alternative splicing and its downregulation by microRNA-222 results in defective exon inclusion impairing the production of muscle-specific isoforms of Coro6, Fxr1 and NACA transcripts. Reconstitution of normal levels of Rbm24 in cells overexpressing microRNA-222 rescues muscle-specific splicing. In conclusion, we have identified a new function of microRNA-222 leading to alteration of myogenic differentiation at the level of alternative splicing, and we provide evidence that this effect is mediated by Rbm24 protein. We built linear models using 2 different experiments and two conditions (miR222 over expression (n=1) and control siRNA(n=2)) with the linear formula (~condition + experiment).

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microRNA-222 regulates muscle alternative splicing through Rbm24 during differentiation of skeletal muscle cells

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The Skeletal Muscle Molecular Clock Regulates Sarcomere Length Through Titin Splicing [1]

Project description:Circadian rhythms have been implicated in regulating skeletal muscle structure and function, but no mechanisms have connected the molecular clock to sarcomeric proteins. We identified an isoform shift in the sarcomeric ruler, titin, and showed that the skeletal muscle molecular clock regulates titin isoform and subsequently sarcomere length through RBM20, an RNA binding protein that controls titin splicing.

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The Skeletal Muscle Molecular Clock Regulates Sarcomere Length Through Titin Splicing [2]

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MBNL splicing factors regulate the microtranscriptome of skeletal muscles (mouse, skeletal muscle, developmental panel)

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Misregulation of alternative splicing of BIN1 leads to T-tubule alterations and muscle weakness in myotonic dystrophy

Project description:Myotonic dystrophes (DM), the most common adult muscular dystrophy, are the first recognized examples of RNA-mediated diseases in which expression of mutant RNAs containing expanded CUG or CCUG repeats interfere with the splicing of other mRNAs. Using whole-genome microarrays, we found that alternative splicing of the BIN1 mRNA is altered in DM skeletal muscle tissues, resulting in the expression of an inactive form of BIN1 deprived of phosphoinositide-binding and membrane-tubulating activities. BIN1 is involved in tubular invaginations of the plasma membrane and is essential for biogenesis of the muscle T-tubules, which are specialized skeletal muscle membrane structures essential to correct excitation-contraction (E-C) coupling. Mutations in the BIN1 gene cause centronuclear myopathy (CNM) that shares some histopathological features with DM, and both diseases are characterized by muscle weakness. Consistent with a loss-of-function of BIN1, muscle T-tubules were altered in DM patients, and membrane tubulation was restored upon expression of the correct splicing form of BIN1 in DM muscle cells. By deciphering the mechanism of BIN1 splicing mis-regulation we demonstrate that the splicing regulator, MBNL1, which is sequestered by expanded CUG and CCUG in DM, binds the BIN1 pre-mRNA and regulates directly its alternative splicing. Finally, reproducing BIN1 splicing alteration in mice is sufficient to reproduce the DM features of T-tubule alterations and muscle weakness. We propose that alteration of BIN1 alternative splicing regulation leads to muscle weakness, a predominant pathological feature of DM. Exon-Array analysis of control and CDM1 muscle primary cultures 10 days of differentiation

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Effect of myotonic dystrophy on pre-mRNA alternative splicing in skeletal muscle

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