Ontology highlight
ABSTRACT:
PROVIDER: PRJNA566148 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:miR-975 overexpression effect on Drosophila cell lines
| PRJNA419952 | ENA
Project description:We overexpressed the conspecific miR-975 in the cell lines derived from multiple Drosophila species (i.e. S2 cells from Drosophila melanogaster; ML82-19a cells from Drosophila simulans and WR-Dv-1 cells from Drosophila virilis). Comparison of the miR-975 effect between different cell lines provide insight into the rewiring of regulatory network through the evolution of new microRNA.
2017-11-30 | GSE107390 | GEO
Project description:We have identified that miR-2b-1 of D. melanogaster causes testicular bulging (a tumour like phenotype) and hence have performed a transcriptomic analysis on these bulged testes. Adult flies overexpressing miR-2b-1 were used to perform transcriptomic analysis to identify the differentially expressed genes.
2022-08-31 | GSE211399 | GEO
Project description:Wolbachia pipientis is a worldwide bacterial parasite of arthropods that infects host germline cells and manipulates host reproduction to increase the ratio of infected females, the transmitting sex of the bacteria. The most common reproductive manipulation, cytoplasmic incompatibility (CI), is expressed as embryonic death in crosses between infected males and uninfected females. Specifically, Wolbachia modify developing sperm in the testes by unknown means to cause a post-fertilization disruption of the sperm chromatin that incapacitates the first mitosis of the embryo. As these Wolbachia-induced changes are stable, reversible, and affect the host cell cycle machinery including DNA replication and chromosome segregation, we hypothesized that the host methylation pathway is targeted for modulation during cytoplasmic incompatibility because it accounts for all of these traits. Here we show that infection of the testes is associated with a 55% increase of host DNA methylation in Drosophila melanogaster, but methylation of the paternal genome does not correlate with penetrance of CI. Overexpression and knock out of the Drosophila DNA methyltransferase Dnmt2 neither induces nor increases cytoplasmic incompatibility. Instead, overexpression decreases Wolbachia titers in host testes by approximately 17%, leading to a similar reduction in CI levels. Finally, strength of CI induced by several different strains of Wolbachia does not correlate with levels of DNA methylation in the host testes. We conclude that DNA methylation mediated by Drosophila's only known methyltransferase is not required for the transgenerational sperm modification that causes CI. Genomic DNA was extracted from pooled samples of Drosophila melanogaster adult testes. One sample from Wolbachia-infected males and one from uninfected males. Bisulfite sequencing was used to determine whether Wolbachia infection affects host DNA methylation in the testes.
2014-12-03 | E-GEOD-63795 | biostudies-arrayexpress
Project description:Whole genome expression analyses reveal little evidence for X chromosome dosage compensation or meiotic inactivation in Drosophila testes, whereas testes-specific transgene reporters suggest a novel form of X chromosome-specific regulation. Gene expression was measured in RNA extracted from adult male and female dissected thorax, and in cells dissected from the apical tip of 2-4 day old adult male testes. Each tissue was assayed on four replicate arrays.
2011-07-21 | E-GEOD-30850 | biostudies-arrayexpress
Project description:The contribution of altered posttranscriptional gene silencing (PTGS) to the development of insulin resistance and type 2 diabetes mellitus so far remains elusive. We have described that expression of microRNAs (miR)-143 and -145 is dysregulated in genetic and dietary mouse models of obesity. Induced transgenic overexpression of miR-143, but not miR-145, causes insulin resistance and impaired insulin-stimulated AKT activation. We used microarrays to analyze the underlying molecular mechanisms of miR-143-mediated development of insulin resistance. miR-143DOX mice (n=3) and wildtype littermate controls (n=3) were treated with doxycycline via the drinking water to induce miR-143 overexpression in the transgenic animals. Primary hepatocytes were isolated for RNA extraction and hybridization on Affymetrix microarrays.
2011-04-08 | E-GEOD-26460 | biostudies-arrayexpress
Project description:Overexpression and inhibition of miR-29 (pre-miR and anti-miR to miR-29b) in murine aortic smooth muscle cells, analysis of their secretome (conditioned media after serum starvation), n=3 for all four groups (pre-miR control, pre-miR-29b, anti-miR control, anti-miR-29b).
2016-05-06 | PXD003938 | Pride
Project description:Ablation of the ATRX chromatin remodeler specifically in forebrain excitatory neurons of mice causes male-specific deficits in long-term spatial memory associated with miR-137 overexpression, transcriptional changes and structural alterations corresponding to pre- and post-synaptic abnormalities.
2020-06-30 | GSE129975 | GEO
Project description:Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus (T2D) and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 1,2,3. MicroRNA (miR)-dependent posttranscriptional gene silencing has recently been recognized to control gene expression in disease development and progression including that of insulin-resistant T2D. MiRs, whose deregulation alters hepatic insulin sensitivity include miR-143, miR-181 and miR-103/107. Here we report that expression of miR-802 is increased in liver of two obese mouse models and of obese human subjects. Inducible transgenic overexpression of miR-802 in mice causes impaired glucose tolerance and attenuates insulin sensitivity, while reduction of miR-802 expression improves glucose tolerance and insulin action. We identify Hnf1b as a target of miR-802-dependent silencing and shRNA-mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signaling and promotes hepatic gluconeogenesis. In turn, hepatic overexpression of Hnf1b improves insulin sensitivity in db/db mice. Thus, the present study defines a critical role for deregulated expression of miR-802 in the development of obesity-associated impairment of glucose metabolism via targeting Hnf1b and assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity.
2012-11-10 | GSE42188 | GEO
Project description:To futher find the gene expression due to the aromatase overexpression in the mouse testis,we have employ whole genome microarray expression profiling as a discovery platform to identify genes compared to the wild type mice. The testes were taken from 5 month old aromatase overexpression mice and WT mice as control. We investigated genes that were significantly upregulated or downregulated in AROM+ mouse testis compared with WT testis. Two groups: 1) total RNA from three 5 month old AROM+ overexpression transgenic mice testes were collected and processed for microarray;2) total RNA from three 5 month old WT mice testes as control.
2014-04-18 | E-GEOD-55254 | biostudies-arrayexpress