Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Structural evolution of the tissue-specific U2AF paralog and alternative splicing factor LS2

ABSTRACT: Structural evolution of the tissue-specific U2AF paralog and alternative splicing factor LS2

PROVIDER: PRJNA657056 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Structural evolution of the tissue-specific U2AF paralog and alternative splicing factor LS2

Project description:To test the effects of mutations in the splicing factor LS2, we expressed GFP-LS2 fusions in Drosophila S2 cells. We then collected polyadenylated RNA and profiled it using high-throughput sequencing and alternative splicing analysis.

2023-08-01 | GSE156213 | GEO

Effect of a SNRPA1-interacting RNA structural element on alternative splicing

Project description:Assessing the influence of RNA structural and sequence variations on SNRPA1-mediated regulation of alternative splicing

2021-03-30 | GSE160955 | GEO

Mechanisms for U2AF to define 3M-bM-^@M-2 splice sites and regulate alternative splicing in the human genome

Project description:The U2AF heterodimer has been well studied for its role in defining functional 3M-bM-^@M-^Y splice sites in pre-mRNA splicing, but many fundamental questions still remain unaddressed regarding the function of U2AF in mammalian genomes. Through genome-wide analysis of U2AF-RNA interactions, we report that U2AF has the capacity to directly define ~88% of functional 3M-bM-^@M-^Y splice sites in the human genome, but numerous U2AF binding events also occur in intronic locations. Mechanistic dissection reveals that upstream intronic binding events interfere with the immediate downstream 3M-bM-^@M-^Y splice site associated with either the alternative exon to cause exon skipping or with the competing constitutive exon to induce exon inclusion. We further demonstrate partial functional impairment with mutations in U2AF35, but not U2AF65, in regulated splicing. These findings reveal the genomic function and regulatory mechanism of U2AF in both normal and disease states. Examination of U2AF heterodimer regulated splicing in Hela cells with CLIP-seq (U2AF65), paired-end RNA-seq (si-NC and si-U2AF65) and RASL-seq (respective three biological replicates of WT, si-NC, si-U2AF65, si-U2AF35, si-NC + pcDNA3.0, si-U2AF65 + pcDNA3.0, and si-U2AF65 + Flag-U2AF35)

2014-10-08 | E-GEOD-61603 | biostudies-arrayexpress

Mechanisms for U2AF to define 3′ splice sites and regulate alternative splicing in the human genome

Project description:The U2AF heterodimer has been well studied for its role in defining functional 3’ splice sites in pre-mRNA splicing, but many fundamental questions still remain unaddressed regarding the function of U2AF in mammalian genomes. Through genome-wide analysis of U2AF-RNA interactions, we report that U2AF has the capacity to directly define ~88% of functional 3’ splice sites in the human genome, but numerous U2AF binding events also occur in intronic locations. Mechanistic dissection reveals that upstream intronic binding events interfere with the immediate downstream 3’ splice site associated with either the alternative exon to cause exon skipping or with the competing constitutive exon to induce exon inclusion. We further demonstrate partial functional impairment with mutations in U2AF35, but not U2AF65, in regulated splicing. These findings reveal the genomic function and regulatory mechanism of U2AF in both normal and disease states.

2014-10-08 | GSE61603 | GEO

WGD paralog evolution

Project description:WGD paralog evolution

| PRJNA743682 | ENA

RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans

Project description:A key step in pre-mRNA splicing is the recognition of 3’ splicing sites by the U2AF large and small subunits, a process regulated by numerous trans-acting splicing factors. How these trans-acting factors interact with U2AF in vivo is unclear. From a screen for suppressors of the temperature-sensitive (ts) lethality of the C. elegans U2AF large subunit gene uaf-1(n4588) mutants, we identified mutations in the RNA binding motif gene rbm-5, a homolog of the tumor suppressor RBM5. rbm-5 mutations can suppress uaf-1(n4588) ts-lethality by loss of function and neuronal expression of rbm-5 was sufficient to rescue the suppression. Transcriptome analyses indicate that uaf-1(n4588) affected the expression of numerous genes and rbm-5 mutations can partially reverse the abnormal gene expression to levels similar to that of wild type. Though rbm-5 mutations did not obviously affect alternative splicing per se, they can suppress or enhance, in a gene-specific manner, the altered splicing of genes in uaf-1(n4588) mutants. Specifically, the recognition of a weak 3’ splice site was more susceptible to the effect of rbm-5. Our findings provide novel in vivo evidence that RBM-5 can modulate UAF-1-dependent RNA splicing and suggest that RBM5 might interact with U2AF large subunit to affect tumor formation.

2018-06-13 | GSE115695 | GEO

Effect of a SNRPA1-interacting RNA structural element on alternative splicing

Project description:Effect of a SNRPA1-interacting RNA structural element on alternative splicing

| PRJNA674898 | ENA

WGD paralog evolution

Project description:Studying the evolution of binding preferences for 30 paralog TF pairs in S.cerevisiae

2022-01-21 | GSE179430 | GEO

Widespread regulated alternative splicing of single codons accelerates proteome evolution

Project description:Thousands of human genes contain introns ending in NAGNAG motifs (N any nucleotide), where both NAGs can function as 3' splice sites, yielding isoforms differing by inclusion/exclusion of just three bases. However, the functional importance of NAGNAG alternative splicing is highly controversial. Using very deep RNA-Seq data from sixteen human and eight mouse tissues, we found that approximately half of alternatively spliced NAGNAGs undergo tissue-specific regulation and that regulated events have been selectively retained: alternative splicing of strongly tissue-specific NAGNAGs was ten times as likely to be conserved between species as for non-tissue-specific events. Further, alternative splicing of human NAGNAGs was associated with an order of magnitude increase in the frequency of exon length changes at orthologous mouse/rat exon boundaries, suggesting that NAGNAGs accelerate exon evolution. Together, our analyses show that NAGNAG alternative splicing constitutes a major generator of tissue-specific proteome diversity and accelerates evolution of proteins at exon-exon boundaries. mRNA-Seq of sixteen human and eight mouse tissues. Supplementary files: human.nagnag.junctions.gff and mouse.nagnag.junctions.gff are the annotation files (in GFF3 format) corresponding to the 'bwtout' mapped reads files linked to the Sample records. Raw data files provided for Samples GSM742937-GSM742952 only.

2012-01-05 | E-GEOD-30017 | biostudies-arrayexpress

RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans

Project description:RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans

| PRJNA475781 | ENA