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RNA-seq of N2a cells treated with 100 nM Dexamethasone for 4 hours +/- siARGLU1

ABSTRACT: ARGLU1 was identified in a screen for new modulators of glucocorticoid signaling in the CNS. RNA-seq of neuronal cells ±siARGLU1 revealed significant changes in the expression and alternative splicing of distinct genes involved in neurogenesis. Treatment with dexamethasone, a GR activator, also induced changes in the pattern of alternatively spliced genes, highlighting an underappreciated global mechanism of glucocorticoid action in neuronal cells. Thus, in addition to its basal role, ARGLU1 links glucocorticoid-mediated transcription and alternative splicing in neural cells, providing new avenues from which to investigate the molecular underpinnings of cognitive stress disorders.

OTHER RELATED OMICS DATASETS IN: PXD012555PXD012406

ORGANISM(S): Mus musculus

PROVIDER: GSE85197 | GEO | 2019/04/17

REPOSITORIES: GEO

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ARGLU1 RIME experiment in N2a cells

Project description:ARGLU1 is a Transcriptional Coactivator and Splicing Regulator Important for Stress Hormone Signaling and Development Stress hormones bind and activate the glucocorticoid receptor (GR) in many tissues including the brain. We identified arginine and glutamate rich 1 (ARGLU1) in a screen for new modulators of glucocorticoid signaling in the CNS. Biochemical studies show that the glutamate rich C-terminus of ARGLU1 coactivates multiple nuclear receptors including the glucocorticoid receptor (GR) and the arginine rich N-terminus interacts with splicing factors and binds to RNA. RNA-seq of neuronal cells depleted of ARGLU1 revealed significant changes in the expression and alternative splicing of distinct genes involved in neurogenesis. Loss of ARGLU1 is embryonic lethal in mice, and knockdown in zebrafish causes neurodevelopmental and heart defects. Treatment with dexamethasone, a GR activator, also induces changes in the pattern of alternatively spliced genes, many of which were lost when ARGLU1 was absent. Importantly, the genes found to be alternatively spliced in response to glucocorticoid treatment were distinct from those under transcriptional control by GR, suggesting an additional mechanism of glucocorticoid action is present in neuronal cells. Our results thus show that ARGLU1 is a novel factor for embryonic development that modulates basal transcription and alternative splicing in neuronal cells with consequences for glucocorticoid signaling.

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SAM68-specific splicing is required for proper selection of alternative 3'UTR isoforms in the nervous system

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