Neoeptesicus furinalis isolate:mEptFur1
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ABSTRACT:
PROVIDER: PRJNA1302024 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Eptesicus furinalis (Argentinian brown bat) genome, mEptFur1, haplotype 2
| PRJNA1302023 | ENA
Project description:Bats are remarkably long-lived for their size with many species living more than 20-40 years, suggesting that they possess efficient anti-aging and anti-cancer defenses. Here we investigated requirements for malignant transformation in primary bat fibroblasts in four bat species - little brown bat (Myotis lucifugus), big brown bat (Eptesicus fuscus), cave nectar bat (Eonycteris spelaea) and Jamaican fruit bat (Artibeus jamaicensis) – spanning the bat evolutionary tree and including the longest-lived genera. We show that bat fibroblasts do not undergo replicative senescence and express active telomerase. Bat cells displayed attenuated stress induced premature senescence with a dampened secretory phenotype. Unexpectedly, we discovered that bat cells could be readily transformed by only two oncogenic perturbations or “hits”: inactivation of either p53 or pRb and activation of oncogenic RASV12. This was surprising because other long-lived mammalian species require up to five hits for malignant transformation. Additionally, bat fibroblasts exhibited increased p53 and MDM2 transcript levels, and elevated p53-dependent apoptosis. The little brown bat showed a genomic duplication of the p53 gene. We hypothesize that bats evolved enhanced p53 activity through gene duplications and transcriptional upregulation as an additional anti-cancer strategy, similar to elephants. In summary, active telomerase and the small number of oncogenic hits sufficient to malignantly transform bat cells suggest that in vivo bats rely heavily on non-cell autonomous mechanisms of tumor suppression.
2025-02-21 | GSE262772 | GEO
Project description:Eptesicus nilssonii (northern bat) genome assembly, mEptNil1, alternate haplotype
| PRJEB62201 | ENA
Project description:Brown adipose tissue (BAT) is a thermogenic organ that protects animals against hypothermia and obesity. BAT derives from the multipotent paraxial mesoderm; however, the identity of embryonic brown fat progenitor cells and regulators of adipogenic commitment are unclear. We identified the transcription factor GATA6 as a selective marker of brown adipogenic progenitor cells. Deletion of Gata6 in the brown fat lineage resulted in a striking loss of BAT. To gain insight into the mechanism by which GATA6 supports BAT development, we performed ChIP-seq for GATA6 from the BAT of embryonic day 15.5 embryos.
2023-07-19 | GSE234012 | GEO
Project description:We performed a genome-wide deep sequencing analysis of the microRNAs abundant in mesenchymal stem cells (MSCs) derived from murine brown adipose tissue and in in vitro differentiated mature brown adipocytes. Several microRNAs were identified as differentially regulated when comparing datasets from MSCs vs. mature fat cells. These microRNAs may have an implication in the regulation of adipogenesis as well as thermogenesis in brown adipose tissue (BAT). Examination of BAT-derived MSCs (BAT-MSC; 1 sample) and in vitro differentiated mature brown fat cells (BAT-DIFF; 1 sample) vertis biotechnologie AG, D-85354 Freising, Germany (library construction and sequencing)
2013-05-28 | E-GEOD-45499 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) and brown adipocytes differentiated in vitro from preadipocytes of PKGI-/- mice vs. WT were compared on a whole genome DNA array
2008-12-31 | GSE11890 | GEO
Project description:Vesper bats (family Vespertilionidae) experienced a rapid adaptive radiation beginning around 36 mya that resulted in the second most species rich mammalian family. Coincident with that radiation was an initial burst of DNA transposon activity that has continued into the present. Deep sequencing of small RNAs from the vespertilionid, Eptesicus fuscus, as well as dog and horse revealed that substantial numbers of novel bat miRNAs are derived from DNA transposons unique to vespertilionids. In fact, 35.9% of Eptesicus-specific miRNAs derive from DNA transposons compared to 2.2 and 5.9% of dog- and horse-specific miRNAs, respectively and targets of several miRNAs are identifiable. Timing of the DNA transposon expansion and the introduction of novel miRNAs coincides remarkably well with the rapid diversification of the family Vespertilionidae. We suggest that the rapid and repeated perturbation of regulatory networks by the introduction of many novel miRNA loci was a factor in the rapid radiation. A testicular tissue sample from dog, horse, and two different Eptesicus fuscus individuals. Four samples total.
2014-05-19 | E-GEOD-47593 | biostudies-arrayexpress
Project description:Brown adipose tissue (BAT) is critical for non-shivering thermogenesis making it a promising therapeutical strategy to combat obesity and metabolic disease. However, the regulatory mechanisms underlying brown fat formation remain incompletely understood. Here, we found SOX4 is required for BAT development and thermogenic program. Depletion of SOX4 in BAT progenitors (Sox4-MKO) or brown adipocytes (Sox4-BKO) resulted in whitened BAT and hypothermia upon acute cold exposure. The reduced thermogenic capacity observed in Sox4-MKO mice increases their susceptibility to diet-induced obesity. Overexpression of SOX4 enhances BAT thermogenesis counteracting diet-induced obesity. Mechanistically, SOX4 activates transcription of EBF2 which determines brown fat fate. Moreover, phosphorylation of SOX4 at S235 by PKA facilitates its nuclear translocation and EBF2 transcription. Further, SOX4 cooperates with EBF2 to activate transcriptional programs governing thermogenic gene expression. These results demonstrate that SOX4 serves as an upstream regulator of EBF2 providing valuable insights into BAT development and thermogenic function maintenance.
2025-03-19 | GSE263446 | GEO
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