Regulation of cellular sterol homeostasis by the oxygen responsive noncoding RNA lincNORS
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ABSTRACT:
PROVIDER: PRJNA640425 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12047294.fastq.gz | Fastqsanger.gz | |||
| SRR12047295.fastq.gz | Fastqsanger.gz | |||
| SRR12047296.fastq.gz | Fastqsanger.gz | |||
| SRR12047297.fastq.gz | Fastqsanger.gz |
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Project description:We hereby provide the initial portrait of lincNORS, a spliced lincRNA generated by the MIR193BHG locus, entirely distinct from the previously described miR-193b-365a tandem. While inducible by low O2 in a variety of cells and associated with hypoxia in vivo, our studies show that lincNORS is subject to multiple regulatory inputs, including estrogen signals. Biochemically, this lincRNA fine-tunes cellular sterol/steroid biosynthesis by repressing the expression of multiple pathway components. Mechanistically, the function of lincNORS requires the presence of RALY, an RNA-binding protein recently implicated in cholesterol homeostasis. We also noticed the proximity between this locus and naturally-occurring genetic variations highly significant for sterol/steroid -related phenotypes, in particular the age of sexual maturation. An integrative analysis of these variants provided a more formal link between these phenotypes and lincNORS, further strengthening the case for its biological relevance.
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Project description:We hereby provide the initial portrait of lincNORS, a spliced lincRNA generated by the MIR193BHG locus, entirely distinct from the previously described miR-193b-365a tandem. While inducible by low O2 in a variety of cells and associated with hypoxia in vivo, our studies show that lincNORS is subject to multiple regulatory inputs, including estrogen signals. Biochemically, this lincRNA fine-tunes cellular sterol/steroid biosynthesis by repressing the expression of multiple pathway components. Mechanistically, the function of lincNORS requires the presence of RALY, an RNA-binding protein recently found to be implicated in cholesterol homeostasis. We also noticed the proximity between this locus and naturally occurring genetic variations highly significant for sterol/steroid-related phenotypes, in particular the age of sexual maturation. An integrative analysis of these variants provided a more formal link between these phenotypes and lincNORS, further strengthening the case for its biological relevance.
| S-EPMC7505984 | biostudies-literature
Project description:We hereby provide the initial portrait of lincNORS, a spliced lincRNA generated by the MIR193BHG locus, entirely distinct from the previously described miR-193b-365a tandem. While inducible by low O2 in a variety of cells and associated with hypoxia in vivo, our studies show that lincNORS is subject to multiple regulatory inputs, including estrogen signals. Biochemically, this lincRNA fine-tunes cellular sterol/steroid biosynthesis by repressing the expression of multiple pathway components. Mechanistically, the function of lincNORS requires the presence of RALY, an RNA-binding protein recently implicated in cholesterol homeostasis. We also noticed the proximity between this locus and naturally-occurring genetic variations highly significant for sterol/steroid -related phenotypes, in particular the age of sexual maturation. An integrative analysis of these variants provided a more formal link between these phenotypes and lincNORS, further strengthening the case for its biological relevance.
2020-06-26 | GSE153292 | GEO
Project description:We hereby provide the initial portrait of lincNORS, a spliced lincRNA generated by the MIR193BHG locus, entirely distinct from the previously described miR-193b-365a tandem. While inducible by low O2 in a variety of cells and associated with hypoxia in vivo, our studies show that lincNORS is subject to multiple regulatory inputs, including estrogen signals. Biochemically, this lincRNA fine-tunes cellular sterol/steroid biosynthesis by repressing the expression of multiple pathway components. Mechanistically, the function of lincNORS requires the presence of RALY, an RNA-binding protein recently implicated in cholesterol homeostasis. We also noticed the proximity between this locus and naturally-occurring genetic variations highly significant for sterol/steroid -related phenotypes, in particular the age of sexual maturation. An integrative analysis of these variants provided a more formal link between these phenotypes and lincNORS, further strengthening the case for its biological relevance.
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Project description:Project Abstract : Trimethylation of histone H3 lysine 4 (H3K4me3) is predominantly associated with transcriptional start sites (TSSs) and is believed to facilitate transcription initiation. Furthermore, H3K4me3 plays a role in defining cell fate and specific cellular functions. Nevertheless, the precise function of H3K4me3 in transcription activation remains a topic of ongoing debate. The Polymerase-associated factor 1 complex (Paf1C), which is integral to various transcription-related cellular processes, consists of five highly conserved subunits: Paf1, Ctr9, Rtf1, Cdc73, and Leo1. While all subunits of Paf1C are indispensable for the maintenance of H3K4 methylation levels, it is noteworthy that strains lacking Leo1 exhibited unaltered levels of H3K4me3. To elucidate the role of H3K4me3, we conducted a transcriptome analysis coupled with ChIP-sequencing of H3K4me3 in cells lacking Leo1. Our research uncovers a distinctive role of Leo1 in yeast, whereby it plays a pivotal role in maintaining sterol homeostasis through the suppression of Upc2 expression. Importantly, this role stands apart from the functions of other Paf1C subunits. H3K4me3 is essential for promoting the expression of sterol uptake genes that are Upc2-dependent when Leo1 is absent. Additionally, Set1 contributes to sterol homeostasis by regulating iron metabolism and mitochondrial functions rather than directly suppressing Upc2 expression. Therefore, our findings reveal a novel role for Leo1 in sterol homeostasis and highlight the importance of H3K4me3 in promoting transcription of response genes required for sterol uptake.
2024-08-01 | GSE244733 | GEO
Project description:Project Abstract : Trimethylation of histone H3 lysine 4 (H3K4me3) is predominantly associated with transcriptional start sites (TSSs) and is believed to facilitate transcription initiation. Furthermore, H3K4me3 plays a role in defining cell fate and specific cellular functions. Nevertheless, the precise function of H3K4me3 in transcription activation remains a topic of ongoing debate. The Polymerase-associated factor 1 complex (Paf1C), which is integral to various transcription-related cellular processes, consists of five highly conserved subunits: Paf1, Ctr9, Rtf1, Cdc73, and Leo1. While all subunits of Paf1C are indispensable for the maintenance of H3K4 methylation levels, it is noteworthy that strains lacking Leo1 exhibited unaltered levels of H3K4me3. To elucidate the role of H3K4me3, we conducted a transcriptome analysis coupled with ChIP-sequencing of H3K4me3 in cells lacking Leo1. Our research uncovers a distinctive role of Leo1 in yeast, whereby it plays a pivotal role in maintaining sterol homeostasis through the suppression of Upc2 expression. Importantly, this role stands apart from the functions of other Paf1C subunits. H3K4me3 is essential for promoting the expression of sterol uptake genes that are Upc2-dependent when Leo1 is absent. Additionally, Set1 contributes to sterol homeostasis by regulating iron metabolism and mitochondrial functions rather than directly suppressing Upc2 expression. Therefore, our findings reveal a novel role for Leo1 in sterol homeostasis and highlight the importance of H3K4me3 in promoting transcription of response genes required for sterol uptake.
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