Analysis of gonadal fat from male control and adipocyte-specific LAMA4 knockout mice
Ontology highlight
ABSTRACT: To determine the transcriptomic effects of LAMA4 loss on adipose tissue structure and gene expression in two dietary paradigms, we assessed gonadal white adipose tissue of male control and adipocyte-specific LAMA4 knockout mice using a Quant-Seq strategy.
Project description:To determine the transcriptomic effects of STAT5 loss on adipose tissue gene expression, we assessed inguinal white adipose tissue of 6-week old male and female control and adipocyte-specific STAT5 knockout mice using a Quant-Seq strategy.
Project description:We used scRNA-seq analysis to investigate the expression profiles of p16high adipocyte progenitor cells compared with p16low adipocyte progenitor cells in the gonadal adipose tissue of aging mice.
Project description:We used bulk RNA-seq analysis to investigate the gene expression patterns of p16high adipocyte progenitor cells compared with p16low adipocyte progenitor cells in the gonadal adipose tissue of tumor bearing mice.
Project description:Identify genes in the gonadal adipose tissue whose expression is under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HMDP comprises classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Parks et al Cell Metabolism 2015. These data are used to identify candidate genes at loci associated with obesity and dietary responsiveness. GWAS for expression of gonadal adipose tissue in inbred strains fed chow diet for 8 weeks followed by high-fat/high-sucrose diet 8 weeks
Project description:In this study we performed RNA sequencing to determine the transcriptome of the gonadal white adipose tissue of pregnant wild type mice. We further assessed, using conditional RankΔFoxn1 knockout mice (which lack expression of Rank in the thymic epithelia), how the expression of the receptor Rank in the thymic medullary epithelia affects the transcriptional program of this tissue during pregnancy, and whether adoptive transfer of natural regulatory Tregs can rescue the alterations observed in the RankΔFoxn1 dams. For this study, we isolated at day E17.5 of pregnancy, the gonadal (peri-uterine) white adipose tissue of wildtype RankWt as well as of RankΔFoxn1 dams pregnant females that were treated at days E0.5-2.5 of pregnancy with either vehicle (PBS) or with 1x105 sorted-purified wild-type natural Tregs isolated from RankWt pregnant E7.5-8.5 donors (denoted as RankΔFoxn1_Treg). For the isolation of viable Tregs for the transplant, we generated RankWt dams that express GFP from the Foxp3 promoter (by crossing to reporter mice), and use the expression of GFP to mark and isolate bona fide Tregs and, in addition, Neuropilin1 to denote the thymic origin of the Tregs. Of note, RankWt as well as of RankΔFoxn1 dams mice also carried the GFP-Foxp3 transgene and where treated with vehicle solution (PBS) at day E0.5-2.5. Total RNA was extracted from the isolated gonadal white adipose tissue of the three described cohorts (RankWt_veh, RankΔFoxn1_veh, and RankΔFoxn1_Treg) and analyzed by Quant-seq. Our study shows how the presence of Rank receptors in the thymic epithelium, functioning via natural Tregs, regulate the inflammatory and metabolic pathways implicated in adipose tissue biology during pregnancy.
Project description:We identified secreted frizzled-related protein-5 (Sfrp5) as a transcript that is upregulated during adipocyte differentiation and that is increased in white adipose tissue (WAT) of obese mice, compared to lean mice. To investigate the function of sFRP5 in adipose tissue biology, we studied sFRP5Q27stop mice, in which ENU mutagenesis was used to create a premature stop codon at Gln27, thereby creating a likely null allele. Male wild-type or Sfrp5 KO (Q27Stop) mice were fed a high-fat diet from the ages of four weeks to twelve weeks. At twelve weeks of age, mice were euthanized. Total RNA was then isolated from gonadal WAT and RNA was analyzed by Affymetrix microarrays. Seven wild-type and eight Sfrp5 KO mice were used.
Project description:Identify genes in the gonadal adipose tissue whose expression is under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HMDP comprises classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Parks et al Cell Metabolism 2015. These data are used to identify candidate genes at loci associated with obesity and dietary responsiveness.
Project description:mRNA expression was compared in between wild type and caveolin-1 knockout livers mRNA expression was compared in between wild type and caveolin-1 knockout gonadal adipose tissue RNA was isolated from livers from male mice in at the light phase RNA was isolated from gonadal adipose tissues from male mice in at the light phase
Project description:Steap4, a highly expressed protein in adipose tissue, has been implicated in metabolic homeostasis. In this study, we generated adipocyte-specific Steap4-deficient mice and observed that Steap4 deficiency led to increased fat mass and severe insulin resistance in a high-fat diet model. Mass spectrometry analysis revealed two classes of Steap4 interactomes: mitochondrial proteins and proteins involved in spliceosome. RNA-seq analysis of white adipose tissue demonstrated that Steap4 deficiency altered RNA splicing patterns with enriched functions in mitochondria. While interactome and transcriptome data implicate a role of Steap4 in mitochondria, Steap4 deficiency indeed impaired mitochondrial respiratory chain complex activity resulting in mitochondrial dysfunction in white adipose tissue. Consistently, brown adipocyte-specific Steap4-deficient mice also showed impaired mitochondrial function, increased whitening of brown adipose tissue, reduced energy expenditure, and exacerbated insulin resistance under HFD conditions. Overall, our findings elucidate the critical role of Steap4 in regulating adipocyte thermogenesis and energy expenditure by modulating mitochondrial function.