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Regulation of retina microexons by srrm3 in zebrafish

ABSTRACT: Regulation of retina microexons by srrm3 in zebrafish

PROVIDER: PRJNA749559 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15242030_1.fastq.gz	Fastqsanger.gz
	SRR15242030_2.fastq.gz	Fastqsanger.gz
	SRR15242031_1.fastq.gz	Fastqsanger.gz
	SRR15242031_2.fastq.gz	Fastqsanger.gz
	SRR15242032_1.fastq.gz	Fastqsanger.gz

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Regulation of retina microexons by srrm3 in zebrafish

Project description:To investigate the role of srrm3 as a regulator of retina microexons (RetMICs) we have sequenced adult retina from WT animals, and enucleated eyes from 5 dpf larvae WT and KO for srrm3.

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Regulation of retina microexons by SRRM3, SRRM4 and MSI1 in human cell lines

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Regulation of retina microexons by srrm3 in zebrafish and by SRRM3, SRRM4 and MSI1 in human cell lines

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Origin and evolution of neural microexons

Project description:The mechanisms by which entire programs of gene regulation emerged during evolution are poorly understood. Neuronal microexons represent the most conserved class of alternative splicing in vertebrates and are critical for proper brain development and function. Here, we discover neural microexon programs in non-vertebrate species and trace their origin to bilaterian ancestors through the emergence of a previously uncharacterized ‘enhancer of microexons' (eMIC) protein domain. The eMIC domain originated as an alternative, neural-enriched splice isoform of the pan-eukaryotic Srrm2/SRm300 splicing factor gene, and subsequently became fixed in the vertebrate and neuronal-specific splicing regulator Srrm4/nSR100 and its paralog Srrm3. Remarkably, the eMIC domain is necessary and sufficient for microexon splicing, and functions by interacting with the earliest components required for exon recognition. The emergence of a novel domain with restricted expression in the nervous system thus resulted in the evolution of splicing programs that contributed to qualitatively expand neuronal molecular complexity in bilaterians.

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Regulation of retina microexons by srrm3 in zebrafish and by SRRM3, SRRM4 and MSI1 in human cell lines

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

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Zebrafish Retina thrb-/- RNA-seq

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MJAY analysis of cerebellar RNA obtained from Srrm3 gene-trapped mice and wild-type mice

Project description:The Bronx waltzer mutation in Srrm4, a gene that encodes a neuronal Ser/Arg (SR)-rich splicing factor, disrupts the expression of several alternative exons specifically in the inner ear. Here we show that the expression of SRRM3 in neurons limits the distribution of SRRM4-dependent splicing. In vitro, SRRM3 and SRRM4 regulated the same alternative exons, yet in vivo Srrm3 deficiency caused neuronal splicing alterations and motor dysfunction, indicating that SRRM3 has non-redundant functions. Mice harboring mutations in both Srrm3 and Srrm4 failed to breathe, and their neuromuscular junctions (NMJ) were malformed. Transcriptome-wide analysis revealed a large network of SRRM3/SRRM4-dependent splicing changes, including the skipping of key exons in the NMJ organizer Agrin. Furthermore, SRRM3/SRRM4 regulated gene expression through neuron-specific switches in chromatin regulatory complexes and by altering the reading frame in several mRNAs. Our findings reveal that the SRRM3/SRRM4 subfamily of SR proteins is central to regulation of the neuronal transcriptome. In this dataset, we include probe-set level data obtained from cerebellar samples. The processed data represent probe-set intensities that have been normalized to gene expression levels.

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