Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355546 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A Long-Range cis-Regulatory Element for Class I Odorant Receptor Genes
| PRJNA355546 | ENA
Project description:Individual olfactory sensory neurons express a single odorant receptor (OR) gene from either class I genes residing in a single cluster on a single chromosome or class II genes spread over multiple clusters on multiple chromosomes. Here, we identify an enhancer element for mouse class I genes, the J element, that regulates class I gene expression of a much larger number of genes and over a much greater genomic distance than known class II gene enhancers. Our data reveal an extraordinary long-range cis-regulatory element that governs the singular class I gene expression and has been phylogenetically preserved to retain a single cluster organization of class I genes in mammals.
2017-07-23 | GSE90700 | GEO
Project description:We developed a systematic statistical method, tTREAT, to identify differentially expressed genes with respect to a predefined FC threshold. The tTREAT approach aims to reduce false discoveries. We applied statistical tests relative to a Fold Change threshold to a dataset about mouse odorant receptor gene expression generated by the NanoString technology. We used mouse strains M-bM-^HM-^FP and M-bM-^HM-^FH that lack the P element and the H element respectively. We also used a mouse strain generated by chromosome engineering (M-bM-^HM-^FOlfr7M-bM-^HM-^F) whereby a 2.4 Mb region is deleted, thus lacking 99 odorant receptor genes. We sought to understand the regulation of the expression of odorant receptor genes by comparing mutant mice to wildtype mice.
2014-01-08 | E-GEOD-53876 | biostudies-arrayexpress
Project description:CAPTURE-3C-seq analysis of cis-element-mediated long-range DNA interactions
| PRJNA387464 | ENA
Project description:Olfactory sensory neurons express just one out of a possible ~1000 odorant receptor genes, reflecting an exquisite mode of gene regulation. In one model, once an odorant receptor is chosen for expression, other receptor genes are suppressed by a negative feedback mechanism, ensuring a stable functional identity of the sensory neuron for the lifetime of the cell. The signal transduction mechanism subserving odorant receptor gene silencing remains obscure, however. Here we demonstrate in the zebrafish that odorant receptor gene silencing is dependent on receptor activity. Moreover, we show that signaling through G protein M-NM-2M-NM-3 subunits is both necessary and sufficient to suppress the expression of odorant receptor genes, and likely acts through histone methylation to maintain the silenced odorant receptor genes in transcriptionally inactive heterochromatin. These results provide new insights linking receptor activity with the epigenetic mechanisms responsible for ensuring the expression of one odorant receptor per olfactory sensory neuron. Total 6 samples were analyzed-3 controls & 3 samples
2013-12-16 | E-GEOD-53334 | biostudies-arrayexpress
Project description:Widespread Long-range Cis-Regulatory Elements in the Maize Genome
| PRJNA492464 | ENA
Project description:Transcriptomic analysis of class I odorant receptor enhancer deletion
| PRJNA552594 | ENA
Project description:Patients suffering from chronic lymphocytic leukemia (CLL) display highly diverse clinical courses ranging from indolent cases to aggressive disease with genetic and epigenetic features resembling this diversity. Here, we developed a comprehensive approach combining a variety of molecular and clinical data to identify translocation events disrupting long-range chromatin interactions and causing cancer-relevant transcriptional deregulation. Thereby, we identified a B cell specific cis-regulatory element restricting the expression of genes in the associated locus, including PRMT5 and DAD1, two factors with oncogenic potential. Examining the role of PRMT5 in CLL identified transcriptional programs associated with pathways of stress tolerance and growth support, maintaining MYC-driven gene expression in vivo and in vitro. Conversely, inhibition of PRMT5 impairs factors involved in DNA-repair and sensitizes cells for apoptosis. Finally, we show that artificial deletion of the regulatory element from its endogenous context resulted in upregulation of corresponding genes, including PRMT5. Furthermore, such disruption renders PRMT5 transcription vulnerable to additional stimuli and subsequently also alters the expression of downstream PRMT5 targets.
2020-08-19 | E-MTAB-8219 | biostudies-arrayexpress
Project description:Patients suffering from chronic lymphocytic leukemia (CLL) display highly diverse clinical courses ranging from indolent cases to aggressive disease with genetic and epigenetic features resembling this diversity. Here, we developed a comprehensive approach combining a variety of molecular and clinical data to identify translocation events disrupting long-range chromatin interactions and causing cancer-relevant transcriptional deregulation. Thereby, we identified a B cell specific cis-regulatory element restricting the expression of genes in the associated locus, including PRMT5 and DAD1, two factors with oncogenic potential. Examining the role of PRMT5 in CLL identified transcriptional programs associated with pathways of stress tolerance and growth support, maintaining MYC-driven gene expression in vivo and in vitro. Conversely, inhibition of PRMT5 impairs factors involved in DNA-repair and sensitizes cells for apoptosis. Finally, we show that artificial deletion of the regulatory element from its endogenous context resulted in upregulation of corresponding genes, including PRMT5. Furthermore, such disruption renders PRMT5 transcription vulnerable to additional stimuli and subsequently also alters the expression of downstream PRMT5 targets.
2020-08-19 | E-MTAB-8203 | biostudies-arrayexpress
Project description:Identification of an LHX target cis-regulatory element through LHX6 ChIP-seq.
| PRJNA291399 | ENA