IlLasMege
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB48330 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Lasiommata megera (wall brown) genome assembly, ilLasMege1
| PRJEB50440 | ENA
Project description:Lasiommata megera (wall brown), genomic and transcriptomic data
| PRJEB48326 | ENA
Project description:Lasiommata megera (wall brown) genome assembly, ilLasMege1, alternate haplotype
| PRJEB50441 | ENA
Project description:Brown adipocytes, muscle and dorsal dermis descend from precursor cells in the dermomyotome, but the factors that regulate commitment to the brown adipose lineage are unknown. Here, we prospectively isolated and determined the molecular profile of embryonic brown preadipose cells. Brown adipogenic precursor activity in embryos was confined to Pdgfrα+, Myf5Cre-lineage-marked cells. RNAseq analysis identified Early B Cell Factor-2 (Ebf2) as one of the most selectively expressed genes in this cell fraction. Importantly, Ebf2-expressing cells purified from Ebf2-GFP embryos or brown fat tissue did not express myoblast or dermal cell markers and uniformly differentiated into brown adipocytes. Interestingly, Ebf2-expressing cells from white fat tissue in adult animals differentiated into brown-like (or beige) adipocytes. Loss of Ebf2 in brown preadipose cells reduced the expression levels of brown preadipose-signature genes, whereas ectopic Ebf2-expression in myoblasts activated brown preadipose-specific genes. Altogether, these results indicate that Ebf2 specifically marks and regulates the molecular profile of brown preadipose cells. Embryonic fibroblasts, isolated from dorsal body wall of E14.5 Myf5-CrE;mTmG embryos, were further fractionated based on the expression of PDGFRα, Itga7 and Myf5-cre (GFP). Total mRNA profiles from Myf5-cre(GFP)+PDGFRα+ and Myf5-cre(GFP)+PDGFRα-Itga7+ cells were generated by deep sequenceing
2014-09-16 | E-GEOD-60441 | biostudies-arrayexpress
Project description:Brown adipocytes, muscle and dorsal dermis descend from precursor cells in the dermomyotome, but the factors that regulate commitment to the brown adipose lineage are unknown. Here, we prospectively isolated and determined the molecular profile of embryonic brown preadipose cells. Brown adipogenic precursor activity in embryos was confined to Pdgfrα+, Myf5Cre-lineage-marked cells. RNAseq analysis identified Early B Cell Factor-2 (Ebf2) as one of the most selectively expressed genes in this cell fraction. Importantly, Ebf2-expressing cells purified from Ebf2-GFP embryos or brown fat tissue did not express myoblast or dermal cell markers and uniformly differentiated into brown adipocytes. Interestingly, Ebf2-expressing cells from white fat tissue in adult animals differentiated into brown-like (or beige) adipocytes. Loss of Ebf2 in brown preadipose cells reduced the expression levels of brown preadipose-signature genes, whereas ectopic Ebf2-expression in myoblasts activated brown preadipose-specific genes. Altogether, these results indicate that Ebf2 specifically marks and regulates the molecular profile of brown preadipose cells. Embryonic fibroblasts, isolated from dorsal body wall of E14.5 Ebf2(GFP)/+ embryos, were further fractionated based on the expression of PDGFRα and Ebf2 (GFP). Affymetrix microarray analysis was prefromed,to compare the gene expression between PDGFRα+ Ebf2(GFP)- and PDGFRα+ Ebf2(GFP)+ cells.
2014-09-16 | E-GEOD-60442 | biostudies-arrayexpress
Project description:Brown fat dissipates energy as heat and protects against obesity. Here, we identified nuclear factor I-A (NFIA) as a novel transcriptional regulator of brown fat by a genome-wide open chromatin analysis of murine brown and white fat followed by motif analysis of brown-fat-specific open chromatin regions. NFIA and the adipogenic master regulator, PPARgamma, co-localize at the brown-fat-specific enhancers. Moreover, the binding of NFIA precedes and facilitates the binding of PPARgamma, leading to increased chromatin accessibility and active transcription. Introduction of NFIA into myoblasts results in brown adipocyte differentiation. Conversely, the brown fat of NFIA knockout mice displays impaired expression of the brown-fat-specific genes and reciprocal elevation of muscle genes. Finally, expression of NFIA and the brown-fat-specific genes is positively correlated in human brown fat. These results indicate that NFIA is a key transcriptional regulator of brown fat and exerts its effects by co-localizing with PPARg at cell-type-specific enhancers.
2017-08-14 | GSE83757 | GEO
Project description:Light plays an important role in the growth and differentiation of Lentinula edodes mycelia, and mycelial morphology is influenced by light wavelengths. The blue light-induced formation of brown film on the vegetative mycelial tissues of L. edodes is an important process. However, the mechanisms of L. edodes’ brown film formation, as induced by blue light, are still unclear. Using a high-resolution liquid chromatography-tandem mass spectrometry integrated with a highly sensitive immune-affinity antibody method, phosphoproteomes of L. edodes mycelia under red- and blue-light conditions were analyzed. A total of 11,224 phosphorylation sites were identified on 2,786 proteins, of which 9,243 sites on 2,579 proteins contained quantitative information. In total, 475 sites were up-regulated and 349 sites were down-regulated in the blue vs red group. To characterize the differentially phosphorylated proteins, systematic bioinformatics analyses, including gene ontology annotations, domain annotations, subcellular localizations, and Kyoto Encyclopedia of Genes and Genomes pathway annotations, were performed. These differentially phosphorylated proteins were correlated with light signal transduction, cell wall degradation, and melanogenesis, suggesting that these processes are involved in the formation of the brown film. Our study provides new insights into the molecular mechanisms of the blue light-induced brown film formation at the post-translational modification level.
2020-10-15 | PXD016536 | Pride
Project description:We performed ChIP-seq to chart genome-wide maps of H3K27me3 in brown preadipocytes and mature brown adipocytes. We observed a subset of brown fat-specific genes, but not common fat genes or white fat-specific genes, possess the H3K27me3 mark in preadipocytes, and this mark is erased in mature adipocytes. H3K27me3 ChIP-seq in brown preadipocytes and mature adipocytes.
2015-12-31 | E-GEOD-55469 | biostudies-arrayexpress
Project description:PR (PRD1-BF1-RIZ1 homologous) domain-containing 16 (PRDM16) drives a brown fat differentiation program, but the mechanisms by which PRDM16 activates brown fat-selective genes have been unclear. Through chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analyses in brown adipose tissue (BAT), we reveal that PRDM16 binding is highly enriched at a broad set of brown fat-selective genes. Importantly, we found that PRDM16 physically binds to MED1, a component of the Mediator complex, and recruits it to superenhancers at brown fat-selective genes. PRDM16 deficiency in BAT reduces MED1 binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes. Together, these data indicate that PRDM16 controls chromatin architecture and superenhancer activity in BAT.
2015-02-10 | GSE63964 | GEO