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Alternative splicing regulated by QKI and RBFOX1 promotes the mesenchymal cell state in breast cancer

ABSTRACT: Alternative splicing regulated by QKI and RBFOX1 promotes the mesenchymal cell state in breast cancer

PROVIDER: PRJNA384253 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5481620_1.fastq.gz	Fastqsanger.gz
	SRR5481620_2.fastq.gz	Fastqsanger.gz
	SRR5481630_1.fastq.gz	Fastqsanger.gz
	SRR5481630_2.fastq.gz	Fastqsanger.gz
	SRR5481621_1.fastq.gz	Fastqsanger.gz

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Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing. The mRNA profiles of control- and QKI-knockdown BEAS2B cells were generated by deep sequencing using Illumina GAIIx sequencer.

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Project description:Rbfox1 regulates the alternative splicing of many transcripts in neurons. We have characterized the Rbfox1-dependent changes in expression and alternative splicing by comparing Rbfox1-KO brain to WT brain. In this dataset, we include the splicing and expression data obtained from dissected WT and Rbfox1 KO mouse brains. 6 total samples were analyzed: brains from 3 WT male mice and 3 Rbfox1 KO male mice, all 1 month of age.

2011-05-16 | E-GEOD-28421 | biostudies-arrayexpress

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Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing.

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Alternative splicing regulated by QKI and RBFOX1 promotes the mesenchymal cell state in breast cancer

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

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MBNL1 and RBFOX1 co-regulate alternative splicing events transcriptome-wide through a conserved buffering mechanism

Project description:Alternative splicing (AS) is an important component of RNA processing controlled by cis- and trans-acting component. Here we investigate modes and mechanisms of AS co-regulation by MBNL1 and RBFOX1. We generated two cell models (human and mouse) whereby the expression of both RBPs can be independently modulated and utilize these cell lines to perform RNAseq and transcriptome wide alternative splicing analysis. Categorization of alternative splicing outcomes of the impacts of RBFOX1 expression on MBNL1 splicing revealed a common co-regulatory mode whereby RBFOX1 buffers MBNL1 dose-dependent splicing regulation by reducing the total range of exon inclusion induced. Overall, our studies define a conserved co-regulatory mechanism through which RBFOX1 and MBNL1 can fine-tune and provide redundancy for AS outcomes.

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RBFOX1 Splicing and Transcriptional Regulation in Neurons

Project description:We used RNA sequencing to identify the RBFOX1 splicing network at a genome-wide level in primary human neural stem cells during differentiation. We observe that RBFOX1 regulates a large set of alternative splicing events implicated in neurogenesis and cell maintenance. Subsequent alterations in gene expression define an additional transcriptional network regulated by RBFOX1 involved in neurodevelopmental pathways remarkably parallel to those affected by splicing. RNA sequencing at a 75bp single-end read scale was performed using polyA-enriched RNA from 5 biological replicates of primary human neural progenitor cell lines generated by lentiviral-mediated knockdown of GFP (control) or RBFOX1 and differentiated for 4 weeks.

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The splicing regulator Rbfox1 (A2BP1) controls neuronal excitation in the mammalian brain

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