Splicing and gene expression changes in human MDAM-MB231 breast cancer cells with TRA2B knockdown
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA565391 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10115919_1.fastq.gz | Fastqsanger.gz | |||
| SRR10115919_2.fastq.gz | Fastqsanger.gz | |||
| SRR10115920_1.fastq.gz | Fastqsanger.gz | |||
| SRR10115920_2.fastq.gz | Fastqsanger.gz | |||
| SRR10115921_1.fastq.gz | Fastqsanger.gz |
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Project description:We have independently knocked down TRA2B and SRSF3 in HEK293 cells to identify the sum of alternative splicing changes that results from depletion of each factor. Each was compared to a control transfection of the hairpin vector alone. In this set, 9 total samples were analyzed. There were three biological replicates for each of three conditions: knockdown control, TRA2B knockdown and SRSF3 knockdown. Arrays were analyzed for gene expression using GeneBase and for alternative splicing using MADS+ and OmniViewer software.
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Project description:Alternative splicing (AS) increases the informational content of the genome and is more prevalent in the brain than in any other tissue. The splicing factor Tra2b (Sfrs10) can modulate splicing inclusion of exons by specifically detecting GAA-rich binding motifs and its absence causes early embryonic lethality in mice. TRA2B has been shown to be involved in splicing processes of Nasp (nuclear autoantigenic sperm protein), MAPT (microtubule associated protein tau) and SMN (survival motor neuron), and is therefore implicated in spermatogenesis and neurological diseases like AlzheimerM-^Rs disease, dementia, ParkinsonM-^Rs disease and spinal muscular atrophy. Here we generated a neuronal-specific Tra2b knock-out mouse that lacks Tra2b expression in neuronal and glial precursor cells by using the Nestin-Cre. Neuronal-specific Tra2b knock-out mice die immediately after birth and show severe abnormalities in cortical development, which are caused by massive apoptotic events in the ventricular layers of the cortex, demonstrating a pivotal role of Tra2b for the developing central nervous system. Using whole brain RNA on exon arrays we identified differentially expressed alternative exons of Tubulin?1 and Shugoshin like2 as in vivo targets of Tra2b. Most interestingly, we found increased expression of the cyclin dependent kinase inhibitor 1a (p21) which we could functionally link to neuronal precursor cells in the affected brain regions. We provide further evidence that the absence of Tra2b causes p21 upregulation and ultimately cell death in NSC34 neuronal-like cells. These findings demonstrate that Tra2b regulates splicing events essential for maintaining neuronal viability during development. Apoptotic events triggered via p21 might not be restricted to the developing brain but could possibly be generalized to the whole organism and explain early embryonic lethality in Tra2b-depleted mice.
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Project description:We have independently knocked down TRA2B and SRSF3 in HEK293 cells to identify the sum of alternative splicing changes that results from depletion of each factor. Each was compared to a control transfection of the hairpin vector alone.
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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.
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