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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RIP-seq)

ABSTRACT: Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RIP-seq)

PROVIDER: PRJNA1046515 | ENA |

REPOSITORIES: ENA

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RIP-seq)

Project description:This study outlines the landscape of isoform usage modulations across major metabolic organs in both mice and monkeys, spanning diverse metabolic states. Our in-depth analysis identify numerous isoform-usage events, intricately influenced by nutrient challenges and largely independent of gene expression regulation. When analysing splicing factor-binding motifs in nutrient-regulated events, HuR emerges as the predominant orchestrator of the isoform network in adipocytes.

2025-02-03 | GSE248965 | GEO

Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

Project description:Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

Project description:Transcriptome modulation is essential for metabolic adaptation to nutrient environments. However, the role of isoform usage, a crucial transcriptome component, is not yet fully understood. This study outlines the landscape of isoform usage modulations across major metabolic organs in both mice and monkeys, spanning diverse metabolic states. Our in-depth analysis identifies numerous isoform-usage events, intricately influenced by nutrient challenges and largely independent of gene expression regulation. Comparative analyses of mice and monkeys highlight hundreds of conserved isoform events that exhibit consistent responses to nutrient challenges across species and correlate with human metabolic traits. When analysing splicing factor-binding motifs in nutrient-regulated events, HuR emerges as the predominant orchestrator of the isoform network in adipocytes, which is validated using an adipose tissue-specific knockout and an Ap2-promoter-driven transgenic mouse model. In summary, our results offer a comprehensive perspective on isoform usage in metabolic regulation, setting a platform for future functional inquiries.

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RNA-seq)

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RNA-seq)

Project description:Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RNA-seq)

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (Monkey-Pacbio)

Project description:Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (Monkey-Pacbio)

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Deciphering isoform switching and specific isoform usage during biofilm lifestyle by Candida glabrata analysed through global transcriptomic approach

Project description:Deciphering isoform switching and specific isoform usage during biofilm lifestyle by Candida glabrata analysed through global transcriptomic approach

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Genetic analysis of isoform usage in the human anti-viral response

Project description:While genetic variants are known to be associated with overall gene abundance in stimulated immune cells, less is known about their effects on alternative isoform usage. Analyzing RNA-seq profiles of monocyte-derived dendritic cells from 243 individuals, we uncovered thousands of unannotated isoforms synthesized in response to influenza infection and type 1 interferon stimulation. We identified more than a thousand quantitative trait loci (QTLs) associated with alternate isoform usage (isoQTLs), many of which are independent of expression QTLs for the same gene. Compared to eQTLs, isoQTLs are enriched for splice sites and untranslated regions, but depleted of sequences upstream of annotated transcription start sites. Both eQTLs and isoQTLs explain a significant proportion of the disease heritability attributed to common genetic variants.

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Differential transcript isoform usage pre- and post-zygotic genome activation in zebrafish

Project description:Zebrafish embryos are transcriptional silent until activation of the zygotic genome during the 10th cell cycle. Onset of transcription is followed by cellular and morphological changes involving cell speciation and gastrulation. Previous genome-wide surveys of transcriptional changes only assessed gene expression levels; however, recent studies have shown the necessity to map isoform-specific transcriptional changes. Here we perform isoform discovery and quantification on transcriptome sequences from before and after zebrafish zygotic genome activation (ZGA). We identify novel isoforms and isoform switches during ZGA for genes related to cell adhesion, pluripotency and DNA methylation. Isoform switching events include alternative splicing and changes in transcriptional start sites and in 3’ untranslated regions. New isoforms are identified even for well-characterized genes such as pou5f1, sall4 and dnmt1. Genes involved in cell-cell interactions such as f11r and magi1 display isoform switches with alterations of coding sequences. We also detect over 1000 transcripts that acquire a longer 3’ terminal exon when transcribed zygotically relative to the maternal transcript counterparts. ChIP-seq data mapped onto skipped exon events reveals a correlation between histone H3K36trimethylation peaks and the skipped exons, suggesting epigenetic marks being part of alternative splicing regulation. The novel isoforms and isoform switches reported here include regulators of the transcriptional, cellular and morphological changes taking place around ZGA. Our data display an array of isoform-related functional changes and represent a valuable resource complementary to existing early embryo transcriptomes. Examination H3K36me3 in zebrafish whole embryos at the Post-MBT stage

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