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MJAY analysis of vestibular macula RNA obtained from Bronx waltzer and control mice.

ABSTRACT: The spontaneous mutant Bronx waltzer (bv) mouse line is characterized by deafness and balance defect. We located the bv mutation to the Srrm4 gene which encodes a regulator of alternative pre-mRNA splicing. We found that Srrm4 is expressed in balance and hearing organs (i.e. in the vestibular maculas and the cochlea). Srrm4 is also expressed in the central nervous system including the cerebellum. To identify potential splicing defects in bv/bv mice, we analyzed RNA samples from the vestibular maculas and cerebellums of bv/bv mice and control (bv/+) littermates, using mouse exon junction microarrays (MJAY). In this dataset, we include probe-set level data obtained from vestibular macula samples. The processed data represent probe-set intensities that have been normalized to gene expression levels (Inorm). Inorm was calculated using batch-corrected data as well as data that were not corrected for a batch effect.

ORGANISM(S): Mus musculus

PROVIDER: GSE33590 | GEO | 2012/10/21

SECONDARY ACCESSION(S): PRJNA154337

REPOSITORIES: GEO

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MJAY analysis of vestibular macula RNA obtained from Bronx waltzer and control mice.

Project description:The spontaneous mutant Bronx waltzer (bv) mouse line is characterized by deafness and balance defect. We located the bv mutation to the Srrm4 gene which encodes a regulator of alternative pre-mRNA splicing. We found that Srrm4 is expressed in balance and hearing organs (i.e. in the vestibular maculas and the cochlea). Srrm4 is also expressed in the central nervous system including the cerebellum. To identify potential splicing defects in bv/bv mice, we analyzed RNA samples from the vestibular maculas and cerebellums of bv/bv mice and control (bv/+) littermates, using mouse exon junction microarrays (MJAY). In this dataset, we include probe-set level data obtained from vestibular macula samples. The processed data represent probe-set intensities that have been normalized to gene expression levels (Inorm). Inorm was calculated using batch-corrected data as well as data that were not corrected for a batch effect. 7 total samples were analyzed: vestibular maculas from 4 heterozygous (bv/+) and 3 homozygous (bv/bv) mouse embryos at E16.5.

2012-10-21 | E-GEOD-33590 | biostudies-arrayexpress

A mutation in the Srrm4 gene causes pre-mRNA splicing defects and deafness in Bronx waltzer mice.

Project description:The spontaneous mutant Bronx waltzer (bv) mouse line is characterized by deafness and balance defect. We located the bv mutation to the Srrm4 gene which encodes a regulator of alternative pre-mRNA splicing. We found that Srrm4 is expressed in balance and hearing organs (i.e. in the vestibular maculas and the cochlea). Srrm4 is also expressed in the central nervous system including the cerebellum. To identify potential splicing defects in bv/bv mice, we analyzed RNA samples from the vestibular maculas and cerebellums of bv/bv mice and control (bv/+) littermates, using mouse exon junction microarrays (MJAY). 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.

2012-10-21 | GSE33589 | GEO

A mutation in the Srrm4 gene causes pre-mRNA splicing defects and deafness in Bronx waltzer mice.

Project description:The spontaneous mutant Bronx waltzer (bv) mouse line is characterized by deafness and balance defect. We located the bv mutation to the Srrm4 gene which encodes a regulator of alternative pre-mRNA splicing. We found that Srrm4 is expressed in balance and hearing organs (i.e. in the vestibular maculas and the cochlea). Srrm4 is also expressed in the central nervous system including the cerebellum. To identify potential splicing defects in bv/bv mice, we analyzed RNA samples from the vestibular maculas and cerebellums of bv/bv mice and control (bv/+) littermates, using mouse exon junction microarrays (MJAY). 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. 8 total samples were analyzed in this series: cerebellums from 4 heterozygous (bv/+) and 4 homozygous (bv/bv) mice at P15.

2012-10-21 | E-GEOD-33589 | biostudies-arrayexpress

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.

2018-07-01 | GSE71479 | GEO

MJAY analysis of cortical RNA obtained from Srrm3-Srrm4 double mutant 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 brain cortex samples. The processed data represent probe-set intensities that have been normalized to gene expression levels.

2018-07-01 | GSE71480 | GEO

Role of SRRM4 in regulating microexons in Circular RNAs in brain tissue

Project description:Studying the role of splicing factor SRRM4 on circular RNAs in human cells

2020-12-07 | GSE159260 | GEO

Role of SRRM4 in regulating microexons in Circular RNAs

Project description:Stduying the role of splicing factor SRRM4 on circular RNAs in human cells

2020-12-07 | GSE148813 | GEO

Conserved role for spliceosomal component PRPF40A in microexon splicing

Project description:Microexons (exons ≤30 nts) are important features of neuronal transcriptomes, but pose mechanistic challenges to the splicing machinery. We previously showed that PRP-40, a component of the U1 spliceosome, is globally required for microexon splicing in C. elegans. Here we show that the homologous PRPF40A is also globally required for microexon splicing in mouse neuroblastoma cells. We find that PRPF40A co-regulates microexons along with SRRM4, a neuron-specific regulator of microexon splicing. The relationship between exon size and dependence on PRPF40A/SRRM4 is distinct, with SRRM4-dependence exhibiting a size threshold (~30 nts) and PRPF40A-dependence exhibiting a graded decrease as exon size increases. Finally, we show that PRPF40A knockdown causes an increase in productive splicing of its spliceosomal binding partner Luc7l by skipping of a small “poison exon.” Similar homeostatic cross-regulation is often observed across paralogous RNA binding proteins. Here we find this concept likewise applies across evolutionarily unrelated but functionally and physically coupled spliceosomal components.

2024-11-05 | GSE267257 | GEO

Genome-wide CRISPR-Cas9 interrogation of splicing networks reveals a mechanism for recognition of autism-misregulated neuronal microexons [SPAR-seq]

Project description:Alternative splicing has critical roles in diverse cellular, developmental and pathological processes. However, the full repertoires of factors that control individual splicing events are not known. We describe a CRISPR-based screening strategy for the systematic identification of genes that control 3-27 nt microexons with functions in nervous system development and that are commonly disrupted in autism. Besides known regulators including nSR100/Srrm4, Rbfox and Ptbp1, approximately 200 additional genes impact microexon splicing. These genes are enriched in genetic links to autism. Two of the screen hits, Srsf11 and Rnps1, preferentially regulate Srrm4-dependent microexons relative to other exons. These factors form mutually stabilizing interactions with Srrm4 that bridge upstream intronic enhancer elements and exonic sequences to activate microexon splicing. Our study thus presents a system for the genome-wide definition of splicing regulatory networks and further reveals a mechanism for the recognition of microexons with critical roles in nervous system development and disorders.

2018-10-12 | GSE120164 | GEO

Genome-wide CRISPR-Cas9 interrogation of splicing networks reveals a mechanism for recognition of autism-misregulated neuronal microexons [RNA-seq]

2018-10-12 | GSE112600 | GEO