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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

ABSTRACT: LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

PROVIDER: PRJNA909613 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22447302_1.fastq.gz	Fastqsanger.gz
	SRR22447302_2.fastq.gz	Fastqsanger.gz
	SRR22447303_1.fastq.gz	Fastqsanger.gz
	SRR22447303_2.fastq.gz	Fastqsanger.gz
	SRR22447304_1.fastq.gz	Fastqsanger.gz

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [RNA-seq]

Project description:The lncRNA EPR (a.k.a BC030870) is highly enriched in the gastrointestinal tract in mice and, more specifically, in the large intestine. We generated conditional EPR knock-out in large intestine e and analyzed genome-wide the gene expression changes by RNA-Seq. Total RNA was extracted from the proximal colon of six control (EPR fl/fl) and six knock-out (EPR cKO) mice. Libraries were constructed and sequenced. Results indicate that EPR knock-out predominantly leads to down-regulation of genes implicated in mucus biogenesis. These results help in explaining the phenotype displayed by EPR cKO mice that is characterized by higher susceptibility to intestinal inflammation and cancer formation.

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis SW480 [RNA-Seq]

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [Hi-C]

Project description:LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [Hi-C]

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [RNA-seq]

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis SW480 [RNA-Seq]

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [Hi-C]

Project description:We have previously shown that EPR favors the interaction between Mettl7a1 promoter and a distal enhancer element. To comprehensively map long-range interactions between promoters and distal regulatory elements that are affected by EPR KO in large intestine, we preformed Promoter capture Hi-C experiments. Crypts were purified from proximal colon of two EPR fl/fl control and two EPR cKO mice. Hi-C libraries were constructed and hybridized with biotinylated RNA probes from the Arima mouse promoter panel designed to hybridize the promoters of 25752 mouse genes. Captured libraries were sequenced and bioinformatically analyzed. Our results indicate that EPR knockout leads to a rewiring of a number of promoter-enhancer interactions.

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

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

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Ribonucleotide excision repair prevents intestinal tumorigenesis

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EPR (BC030870) ChIP-Seq analysis in NMuMG mouse mammary gland

Project description:EPR, a lncRNA present in the chromatin fraction of NMuMG cells, controls proliferation and fate determination in mammary gland cells. We wanted to define if EPR overexpression in NMuMG cells affects the landcape of two histone activation marks (H3K4me3 and H3K27ac).

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LncRNA EPR-induced METTL7A1 modulates target gene translation

Project description:EPR is a long non-coding RNA (lncRNA) that controls cell proliferation in mammary gland cells by regulating gene transcription. Here, we report on Mettl7a1 as a direct target of EPR. We show that EPR induces Mettl7a1 transcription by rewiring three-dimensional chromatin interactions at the Mettl7a1 locus. Our data indicate that METTL7A1 contributes to EPR-dependent inhibition of TGF-β signaling. METTL7A1 is absent in tumorigenic murine mammary gland cells and its human ortholog (METTL7A) is downregulated in breast cancers. Importantly, re-expression of METTL7A1 in 4T1 tumorigenic cells attenuates their transformation potential, with the putative methyltransferase activity of METTL7A1 being dispensable for its biological functions. We found that METTL7A1 localizes in the cytoplasm whereby it interacts with factors implicated in the early steps of mRNA translation, associates with ribosomes, and affects the levels of target proteins without altering mRNA abundance. Overall, our data indicates that METTL7A1 —a transcriptional target of EPR— modulates translation of select transcripts.

2022-08-12 | PXD034398 | Pride

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