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A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing

ABSTRACT: A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing

PROVIDER: PRJNA755649 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15502200_1.fastq.gz	Fastqsanger.gz
	SRR15502200_2.fastq.gz	Fastqsanger.gz
	SRR15502170_1.fastq.gz	Fastqsanger.gz
	SRR15502170_2.fastq.gz	Fastqsanger.gz
	SRR15502171_1.fastq.gz	Fastqsanger.gz

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A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [RNA-Seq]

Project description:A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [RNA-Seq]

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A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [CLEAR-CLIP]

Project description:A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [CLEAR-CLIP]

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A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing.

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A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [RNA-Seq]

Project description:miRNAs are regulatory transcripts established as repressors of mRNA stability and translation. Here we demonstrate that an oncomiR-10b binds to U6 snRNA, a core component of the spliceosomal machinery. We provide evidence of direct binding between miR-10b and U6, in situ visualizations of miR-10b and U6 co-localization in glioma cells and tumor tissues, and biochemical co-isolation of miR-10b with the components of the spliceosome. We further demonstrate that miR-10b modulates U6 N-6-adenosine methylation and pseudouridylation, U6 binding to splicing factors SART3 and PRPF8, and regulates U6 stability, conformation, and levels. The effects on U6 result in splicing alterations, illustrated by the altered ratio of the isoforms of a small GTPase CDC42, reduced overall CDC42 levels, and downstream CDC42 -mediated effects on cell viability. We, therefore, present an unexpected intersection of the miRNA and splicing machineries and a new nuclear function for a cancer-associated miRNA.

2022-01-19 | GSE182280 | GEO

A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing [CLEAR-CLIP]

2022-01-19 | GSE182281 | GEO

A nuclear function for an oncogenic microRNA as a modulator of snRNA and splicing

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

2022-01-19 | GSE182282 | GEO

Novel RNA-binding Proteins Bind U1 snRNA to Promote Splicing of Weak 5' Splice Sites

Project description:Removal of introns during pre-mRNA splicing, which is central to gene expression, initiates by base pairing of U1 snRNA with a 5' splice site (5'SS). In mammals, many introns contain weak 5'SSs that are not efficiently recognized by the canonical U1 snRNP, suggesting alternative mechanisms exist. Here, we develop a cross-linking immunoprecipitation coupled to a high-throughput sequencing method, BCLIP-seq, to identify NRDE2 (Nuclear RNAi defective-2) and CCDC174 (Coiled-Coil Domain-Containing 174) as novel RNA-binding proteins in mouse ES cells that associate with U1 snRNA and unspliced 5'SSs. Both proteins bind directly to U1 snRNA independently of canonical U1 snRNP specific proteins, and they are required for the selection and effective processing of weak 5'SSs. Our results reveal that mammalian cells use non-canonical splicing factors bound directly to U1 snRNA to effectively select suboptimal 5'SS sequences in hundreds of genes, promoting proper splice site choice and accurate pre-mRNA splicing.

2023-09-07 | PXD029392 | Pride

Novel RNA-binding Proteins Bind U1 snRNA to Promote Splicing of Weak 5' Splice Sites

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METTL4 catalyzes m6Am methylation in U2 snRNA to regulate pre-mRNA splicing

Project description:N6-methylation of 2’-O-methyladenosine (Am) in RNA occurs in eukaryotic cells to generate N6,2’-O-dimethyladenosine (m6Am). Identification of the methyltransferase responsible for m6Am catalysis has accelerated studies on the function of m6Am in RNA processing. While m6Am is generally found in the first transcribed nucleotide of mRNAs, the modification is also found internally within U2 snRNA. However, the writer required for catalyzing internal m6Am formation had remained elusive. By sequencing transcriptome-wide RNA methylation at single-base-resolution, we identified human METTL4 as the writer that directly methylates Am at U2 snRNA position 30 into m6Am. We found that METTL4 localizes to the nucleus and its conserved methyltransferase catalytic site is required for U2 snRNA methylation. By sequencing human cells with overexpressed Mettl4, we determined METTL4’s in vivo target RNA motif specificity. In the absence of Mettl4 in human cells, U2 snRNA lacks m6Am thereby affecting a subset of splicing events that exhibit specific features such as overall 3’ splice-site weakness with certain motif positions more affected than others. This study establishes that METTL4 methylation of U2 snRNA regulates splicing of specific pre-mRNA transcripts.

2020-08-17 | GSE144745 | GEO

Human U2 snRNA BSL sequence mediates splicing efficiency driven by branchpoint sequence complementarity

Project description:To investigate the global effects of perturbing U2 snRNA sequence on splicing and gene expression, we carried out transcriptomic analysis of HEK293T cell lines stably expressing U2 snRNA mutants C28U in the branchpoint interacting stem loop or T34A/ A35C/G36T to create an orthogonal branch point recognition sequence. With both mutants, the expression of many genes is generally repressed, potentially by nonsense mediated decay (NMD) arising from a global decrease in splicing efficiency. However, we also see upregulation of genes important for pre-mRNA processing, translation and protein folding. In several cases, the upregulation of certain genes can be linked to a shift in alternative splicing that favors the productive isoform relative to an NMD-targeted isoform.

2026-02-13 | GSE303759 | GEO

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