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An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (iCLIP-seq)

ABSTRACT: An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (iCLIP-seq)

PROVIDER: PRJNA984309 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24941037.fastq.gz	Fastqsanger.gz
	SRR24941038.fastq.gz	Fastqsanger.gz
	SRR24941039.fastq.gz	Fastqsanger.gz

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Similar Datasets

An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (iCLIP-seq)

Project description:Alternative splicing-induced inclusion of poison exons containing in-frame stop codons is a mechanism that can be used to attenuate gene expression. Poison exon have been implicated in cancer, but how they operate within the context of normal development and physiology is poorly understood. Several splicing regulator genes, including Tra2b, contain ultra-conserved poison exons that function within regulatory loops to fine-tune their activity. To investigate the physiological role of poison exons in vivo, we created mice lacking either Tra2b or its poison exon, specifically during spermatogenesis to reveal both are essential for male fertility. The mouse Tra2b gene is essential for mitotic proliferation of germ cells, whereas, in contrast, the Tra2b poison exon is critically required during meiosis and not needed by mitotically proliferating cell populations within the germline. Poison exon deletion causes infertility, with a block in male meiotic prophase where Tra2β protein expression levels normally increase. Deletion of the Tra2b poison exon changes expression patterns of genes important for meiosis and splicing patterns of Tra2β target exons, suggesting Tra2b poison exon splicing prevents meiotic cells accumulating toxic levels of Tra2b expression. Our data provide a new physiological explanation for Tra2b poison exon ultra-conservation and indicate the importance of evaluating poison exon function within a physiological context.

2024-12-19 | GSE235083 | GEO

An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (RNA-seq)

2024-12-19 | GSE235084 | GEO

An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice

Project description:An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice

| PRJNA984307 | ENA

An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (RNA-seq)

Project description:An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice (RNA-seq)

| PRJNA984310 | ENA

An essential role for the ultra-conserved poison exon of Tra2b in fertility in mice

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

2024-12-19 | GSE235085 | GEO

An ultra-conserved poison exon in the Tra2b gene encoding a splicing activator is essential for male fertility and meiotic cell division

Project description:The cellular concentrations of splicing factors (SFs) are critical for controlling alternative splicing. Most serine and arginine-enriched (SR) protein SFs regulate their own concentration via a homeostatic feedback mechanism that involves regulation of inclusion of non-coding 'poison exons' (PEs) that target transcripts for nonsense-mediated decay. The importance of SR protein PE splicing during animal development is largely unknown despite PE ultra-conservation across animal genomes. To address this, we used mouse genetics to disrupt an ultra-conserved PE in the Tra2b gene encoding the SR protein Tra2β. Focussing on germ cell development, we found that Tra2b PE deletion causes azoospermia due to catastrophic cell death during meiotic prophase. Failure to proceed through meiosis was associated with increased Tra2b expression sufficient to drive aberrant Tra2β protein hyper-responsive splice patterns. Although critical for meiotic prophase, Tra2b PE deletion spared earlier mitotically active germ cells, even though these still required Tra2b gene function. Our data indicate that PE splicing control prevents the accumulation of toxic levels of Tra2β protein that are incompatible with meiotic prophase. This unexpected connection with male fertility helps explain Tra2b protein PE ultra-conservation and indicates the importance of evaluating PE function in animal models.

| S-SCDT-10_1038-S44318-024-00344-6 | biostudies-other

Tra2b's Ultraconserved Poison Exon relays TCR stimulation to shape T cell fate [PEKOSeq]

Project description:Analysis of transcript changes with enough depth for evaluation of splicing changes between scrambled control CD8+ T or Tra2b-PE KO CD8+ T cells from mice

2024-06-01 | GSE267601 | GEO

Tra2b's Ultraconserved Poison Exon relays TCR stimulation to shape T cell fate [ASO_RNASeq]

Project description:Analysis of transcript changes with enough depth for evaluation of splicing changes between CD8+ T cells from human donor PBMCs receiving no stimulation,CD3/CD28 stimulation plus scrambled ASO, or CD3/CD28 plus Tra2b-PE ASO

2024-06-01 | GSE267586 | GEO

Tra2b's Ultraconserved Poison Exon relays TCR stimulation to shape T cell fate [CLIP-seq]

Project description:Analysis of Tra2b binding sites in Naïve and Effector CD8+ T cells from spleens and lymph nodes of OT-I mice unstimulated or stimulated with SIINFEKL peptide + anti-OX40/41BB for 4 days

2024-06-01 | GSE267587 | GEO

Investigation into human Tra2 protein-dependent splicing in MDA-MB-231 cells using iCLIP and RNA-seq

Project description:Alternative splicing—the production of multiple mRNA isoforms from a single gene—is regulated in part by RNA-binding proteins (RBPs). While the RBPs Tra2? and Tra2? have both been implicated in the regulation of alternative splicing, their relative contribution to this process are not well understood. Here we use iCLIP to identify Tra2? target exons in MDA-MB-231 cells. We find that simultaneous—but not individual—depletion of Tra2? and Tra2? induces substantial shifts in the splicing pattern of endogenous Tra2? target exons identified by iCLIP. We next use RNA-seq following joint Tra2 protein depletion to comprehensively identify Tra2 protein-dependent exons in MDA-MB-231 cells. Endogenous Tra2? binding sites were mapped across the MDA-MB-231 cell transcriptome in biological triplicate iCLIP experiments. RNA-seq was performed using three biological replicates of negative control siRNA treated MDA-MB-231 cells and three biological replicates of TRA2A and TRA2B siRNA treated MDA-MB-231 cells.

2014-07-12 | E-GEOD-59335 | biostudies-arrayexpress

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