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.
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.
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).
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.