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MRNA splicing is modulated by intronic microRNAs

ABSTRACT: mRNA splicing is modulated by intronic microRNAs

PROVIDER: PRJNA988817 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25056300_1.fastq.gz	Fastqsanger.gz
	SRR25056300_2.fastq.gz	Fastqsanger.gz
	SRR25056301_1.fastq.gz	Fastqsanger.gz
	SRR25056301_2.fastq.gz	Fastqsanger.gz
	SRR25056302_1.fastq.gz	Fastqsanger.gz

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mRNA splicing is modulated by intronic microRNAs

Project description:Splicing of transcripts is catalyzed by the spliceosome, a mega-complex consisting of hundreds of proteins and five snRNAs, which employs direct interactions. When U1 snRNA forms high affinity binding, namely more than eight base-pairs, with the 5’SS, the result is usually a suppressing effect on the splicing activity. This likely occurs due to the inefficient unwinding of U1/5’SS base-pairing, or other regulatory obstructions. Here we show in vitro and in patient-derived cell lines that pre-microRNAs can modulate the splicing reaction by interacting with U1 snRNA. This leads to reduced binding affinity to the 5’SS, and hence promotes the inclusion of exons containing 5’SS, despite sequence-based high affinity to U1. Application of the mechanism resulted in correction of the splicing defect in the disease-causing VCAN gene from an individual with Wagner syndrome. This pre-miRNA/U1 interaction can regulate the expression of alternatively spliced exons, thus extending the scope of mechanisms regulating splicing.

2023-09-21 | GSE236090 | GEO

Systematic analysis of intronic microRNAs reveals cooperativity within the multi-component FTX locus to promote colon cancer development

Project description:Approximately half of all microRNAs reside within intronic regions and are often co-transcribed with their host genes. However, most studies on intronic microRNAs focus on individual microRNAs, and conversely most studies on protein-coding and non-coding genes frequently ignore any intron-derived microRNAs. We hypothesize that the individual components of such multi-genic loci may play cooperative or competing roles in driving disease progression, and that examining the combinatorial effect of these components would uncover deeper insights into their functional importance. To address this, we perform systematic analyses of intronic microRNA:host loci in colon cancer. We observe that the FTX locus, comprising of a long non-coding RNA FTX and multiple intronic microRNAs, is highly upregulated in cancer and demonstrate that cooperativity within this multi-component locus promotes cancer growth. In addition, we show that FTX interacts with DHX9 and DICER and delineate its novel roles in regulating A-to-I RNA editing and microRNA expression. These results show for the first time that a long non-coding RNA can regulate A-to-I RNA editing, further expanding the functional repertoire of long non-coding RNAs. We further demonstrate the inhibitory effects of intronic miR-374b and -545 on the tumor suppressors PTEN and RIG-I to enhance the proto-oncogenic PI3K-AKT signaling. Finally, we show that intronic miR-421 may exert an autoregulatory effect on miR-374b and -545. Taken together, our data unveil the intricate interplay between intronic microRNAs and their host transcripts in the modulation of key signaling pathways and disease progression, adding new perspectives to the functional landscape of multi-genic loci.

2021-01-05 | PXD021823 | Pride

Intronic tRNAs of mitochondrial origin regulate constitutive and alternative splicing

Project description:Background: The presence of nuclear mitochondrial DNA (numtDNA) has been reported within several nuclear genomes. Next to mitochondrial protein coding genes, numtDNA sequences also encode for mitochondrial tRNA genes. However, the biological roles of numtDNA, remain elusive. Results: Employing in silico analysis we identify 281 mitochondrial tRNA homologs in the human genome, which we term nimtRNAs (nuclear intronic mitochondrial-derived tRNAs), being contained within introns of 76 nuclear host genes. Despite base changes in nimtRNAs when compared to their mtRNA homologs, a canonical tRNA cloverleaf structure is maintained. To address potential functions of intronic nimtRNAs, we insert them into introns of constitutive and alternative splicing reporters and demonstrate that nimtRNAs promote pre-mRNA splicing, dependent on number and positioning of nimtRNA genes and splice site recognition efficiency. A mutational analysis reveals that the nimtRNA cloverleaf structure is required for the observed splicing increase. Utilizing a CRISPR/Cas9 approach we show that a partial deletion of a single endogenous nimtRNALys within intron 28 of the PPFIBP1 gene decreases inclusion of the downstream located exon 29 of the PPFIBP1 mRNA. By employing a pull-down approach followed by mass spectrometry, a 3’-splice site associated protein network is identified, including KHDRBS1, which we show directly interacts with nimtRNATyr by an electrophoretic mobility shift assay. Conclusions: We propose that nimtRNAs, along with associated protein factors, can act as a novel class of intronic splicing regulatory elements in the human genome by participating in the regulation of splicing.

2020-10-28 | PXD022204 | Pride

pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts

Project description:pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts

| PRJNA972004 | ENA

pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [II]

Project description:pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [II]

| PRJNA858869 | ENA

pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

Project description:pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

| PRJNA858771 | ENA

Intronic Non-CG DNA Hydroxymethylation and Alternative mRNA Splicing in Honey Bees

Project description:Intronic Non-CG DNA Hydroxymethylation and Alternative mRNA Splicing in Honey Bees

| PRJNA219484 | ENA

New strategies for the identification of intronic variants related to splicing events in pancreas cancer [iCELL8]

Project description:Most clinical diagnostic settings and genomic research focus almost exclusively on coding regions and essential splice sites, mostly ignoring non-coding variants. Indeed, the investigation of intronic mis-splicing variants interpreting mechanisms to disease-associated splicing events requires both genomic and transcriptomic data. Unfortunately, there are not many datasets where both are available, leading to the understanding of intronic variants in diseases full of gaps. In this study, we present for the first time a full-length single nuclei RNA-sequencing (snRNA-Seq) approach improving the proper investigation of pathogenic mis-splicing intronic variants in pancreatic cancer showing its contribution to abnormal splicing changes and their transcriptional effects. Finally, we discuss the demands of further machine learning-based methods to process the growing number of single cell data and to enhance the precision and recall.

2024-05-10 | GSE229006 | GEO

New strategies for the identification of intronic variants related to splicing events in pancreas cancer [RNA-Seq]

2024-05-08 | GSE228844 | GEO

pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

Project description:Combinatorially, intron excision within a given nascent transcript could proceed down any of thousands of paths, each of which would expose different dynamic landscapes of cis-elements and contribute to alternative splicing. In this study, we found that post-transcriptional multi-intron splicing order in human cells is largely predetermined, with most genes spliced in one or a few predominant orders. Strikingly, these orders were conserved across cell types and stages of motor neuron differentiation. Introns flanking alternatively spliced exons were frequently excised last, after their neighboring introns. Perturbations to the spliceosomal U2 snRNA altered the preferred splicing order of many genes, and these alterations were associated with the retention of other introns in the same transcript. In one gene, early removal of specific introns was sufficient to induce delayed excision of three proximal introns, and this delay was caused by two distinct cis-regulatory mechanisms. Together, our results demonstrate that multi-intron splicing order in human cells is predetermined, is influenced by a component of the spliceosome and ensures splicing fidelity across long pre-mRNAs.

2023-05-14 | GSE208197 | GEO

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