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Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) during hippocampal Long-Term Potentiation (LTP) [3'READS]

ABSTRACT: This study was aimed at elucidating the mechanisms underlying activity-dependent gene regulation during LTP of mouse hippocampal CA3-CA1 synapses. Deep sequencing of the 3’ end of transcripts allowed to identify changes in APA induced 1 hour and 3 hours after LTP induction. We detected APA changes that only affected the 3'UTR (3'UTR-APA events) and APA changes that also affected the coding sequence (CDS-APA events).

ORGANISM(S): Mus musculus

PROVIDER: GSE84643 | GEO | 2018/02/22

REPOSITORIES: GEO

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Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) During Hippocampal Long-Term Potentiation (LTP) [RNA-Seq]

Project description:This study was aimed at elucidating the mechanisms underlying activity-dependent gene regulation during long-term potentiation (LTP) of mouse hippocampal CA3-CA1 synapses. Transcriptome analysis allowed to identify changes in gene expression and alternative splicing induced 1 hour and 3 hours after LTP induction.

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Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) During Hippocampal Long-Term Potentiation (LTP)

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CPSF role on APA regulation

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DNA-methylation of LTP-associated genes.

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Activity-Dependent Regulation of Alternative Cleavage and Polyadenylation (APA) During Hippocampal Long-Term Potentiation (LTP)

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

2018-02-22 | GSE84644 | GEO

Expression data from APA+ and APA- progenitors and SSEA5+ human pluripotent stem cells

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Alternative polyadenylation alters protein dosage by switching between intronic and 3' UTR sites

Project description:Alternative polyadenylation (APA) creates distinct transcripts from the same gene by cleaving the pre-mRNA at poly(A) sites that can lie within the 3' UTR, introns, or exons. Most studies focus on APA within the 3' UTR, but here we show that CPSF6 insufficiency alters protein levels and causes a developmental syndrome by deregulating APA throughout the transcript. In neonatal humans and zebrafish larvae, CPSF6 insufficiency shifts poly(A) site usage between the 3'UTR and internal sites in a pathway-specific manner. Genes associated with neuronal function undergo mostly intronic APA, reducing their expression, while genes associated with heart and skeletal function mostly undergo 3' UTR APA and are upregulated. This suggests that, in healthy conditions, cells toggle between internal and 3'UTR APA to modulate protein expression.

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