Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA95301 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the RNA expression of the mature brown fat from 6 week old wild type (WT) and PHOSPHO1 knockout (KO) mice. Mature brown fat was isolated from brown adipose tissue after collagenase digestion. Increased expression of mitochondrial genes is found in KO brown fat.
2020-07-08 | GSE129020 | GEO
Project description:Global RNA sequencing analysis of brown fat (BAT), inguinal white fat (iWAT), liver and muscle (quadriceps) of high-fat diet fed WT, FGF21 KO, UCP1 KO and UCP1/FGF21 double KO mice.
2019-11-05 | GSE122167 | GEO
Project description:PKGI KO vs. WT brown adipocytes and brown adipose tissues
| PRJNA117215 | ENA
Project description:To investigate the specific role of PGC-1 coactivators in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1alpha. We could then efficiently knockdown PGC-1beta expression by shRNA expression. Loss of PGC-1alpha did not alter brown fat differentiation but severly reduced the induction of thermogenic genes. In order to assess the specific requirement for PGC-1± in the global transcriptional response to cAMP, we used Affymetrix arrays to compare the sets of genes induced in response to a 4 hr dbcAMP treatment in differentiated wt and KO cells. This analysis revealed that 88 genes were induced more than 3-fold in the wt cells; of these, 54 (61% of total) were similarly increased in both wt and KO. However, 28 genes (32% of total) were decreased by at least 50% in the KO cells compared to wt cells. These data were confirmed by quantitative PCR for a subset of genes. These data indicate that PGC-1± is required for proper expression of approximately one third of the genes induced in response to cAMP in brown fat cells, but this set of sensitive genes is enriched in those involved in adaptative thermogenesis. Experiment Overall Design: WT and PGC-1alpha KO brown preadipocytes were differentiated into mature brown adipocytes for seven days. Cells were then treated with dibutyryl cAMP for four hours. Two replicates were made for each condition: WT non treated, WT treated with cAMP, KO non treated, KO treated with cAMP. Transcription profiling of wild type and PGC-1 alpha knockout mouse mature brown adipocytes treated with dibutyryl cAMP to investigate the specific role of PGC-1 coactivators in brown fat cells
2007-11-27 | E-GEOD-5041 | biostudies-arrayexpress
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
2019-05-07 | GSE129060 | GEO
Project description:RNAseq on WT and Meteor KO Embryonic Stem Cells and day3 differentiated cells
| PRJNA401996 | ENA
Project description:Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1±. We could then efficiently knockdown PGC-1β expression by shRNA expression. Loss of PGC-1± did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. Cells deficient in either PGC-1α or PGC-1β coactivators showed a small decrease in the differentiation-dependant program of mitochondrial biogenesis and respiration; however, this increase in mitochondrial number and function was totally abolished during brown fat differentiation when both PGC-1± and PGC-1 were deficient. These data show that PGC-1± is essential for brown fat thermogenesis but not brown fat differentiation, and the PGC-1 coactivators play an absolutely essential but complementary function in differentiation-induced mitochondrial biogenesis. Affymetrix microarray analysis of total RNA from wt, PGC-1± KO and PGC-1± KO; cells expressing an RNAi specific for PGC-1 knockdown was performed. Of the 461; mitochondrial genes analyzed, 181 were found to be at least 20% different between wt; and defective PGC-1± and β adipocytes (p < 0.05). More than 85% of these genes were downregulated in cells deficient for PGC-1alpha and PGC-1beta. Experiment Overall Design: Brown preadipocytes that were either WT, KO for PGC-1alpha, or KO for PGC-1alpha and deficient for PGC-1beta (knockdown through siRNA expression) were differentiated for seven days. RNA was made from biological replicates of the three different types of brown adipocytes (WT, KO expressing a control siRNA, KO expressing a siRNA specific for PGC-1beta knockdown).
2007-11-27 | E-GEOD-5042 | biostudies-arrayexpress
Project description:To investigate the specific role of PGC-1 coactivators in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1alpha. We could then efficiently knockdown PGC-1beta expression by shRNA expression. Loss of PGC-1alpha did not alter brown fat differentiation but severly reduced the induction of thermogenic genes. In order to assess the specific requirement for PGC-1α in the global transcriptional response to cAMP, we used Affymetrix arrays to compare the sets of genes induced in response to a 4 hr dbcAMP treatment in differentiated wt and KO cells. This analysis revealed that 88 genes were induced more than 3-fold in the wt cells; of these, 54 (61% of total) were similarly increased in both wt and KO. However, 28 genes (32% of total) were decreased by at least 50% in the KO cells compared to wt cells. These data were confirmed by quantitative PCR for a subset of genes. These data indicate that PGC-1α is required for proper expression of approximately one third of the genes induced in response to cAMP in brown fat cells, but this set of sensitive genes is enriched in those involved in adaptative thermogenesis. Keywords: thermogenic gene program
2006-07-06 | GSE5041 | GEO
Project description:We investigated the effect of Bola3 in brown fat mitochondria. From Bola3 knockout (KO) mice and wild type (WT) control, we isolated mitochondria from brown fat for proteome profiling. We applied 250 ng peptides for LC/MS/MS analysis using label-free quantification coupled match-between-run approach.
2019-07-18 | PXD014143 | JPOST Repository
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature