Project description:The purpose of this experiment is to respond to the NIGMS mandate to screen Core F generated glycosyltransferase KO mice in Core E and Core C. The goal is to screen several tissues for gene expression changes in ST6GalNAc2 KO mice and B4GalNT1/B4GalNT2 double KO mice relative to C75 Wild Type controls. Tissues for Core E analysis were selected by mining public databases including the NIH GEO database for tissues that expressed the KO genes at moderate to high levels.
Project description:The purpose of this experiment is to respond to the NIGMS mandate to screen Core F generated glycosyltransferase KO mice in Core E and Core C. The goal is to screen several tissues for gene expression changes in ST6GalNAc2 KO mice and B4GalNT1/B4GalNT2 double KO mice relative to C75 Wild Type controls. Tissues for Core E analysis were selected by mining public databases including the NIH GEO database for tissues that expressed the KO genes at moderate to high levels. Results from Core E gene expression analysis are then used to help Core C select tissues to follow up with glycan analysis on in each of the KO mice. For the ST6GalNAc2 KO mouse we selected: Brain, Small Intestine, Lymph Node and Thyroid for analysis. For the B4GalNT1/B4GalNT2 double KO mouse we selected: Kidney, Mammary Gland, Thymus and Testes for analysis. Wild type tissues were analyzed in parellel.
Project description:Peroxisomes are versatile single membrane-enclosed cytoplasmic organelles, involved in reactive oxygen species (ROS) and lipid metabolism and diverse other metabolic processes. Peroxisomal disorders result from mutations in Pex genes-encoded proteins named peroxins (PEX proteins) and single peroxisomal enzyme deficiencies. The PEX11 protein family (α, β, and γ isoforms) plays an important role in peroxisomal proliferation and fission. However, their specific functions and the metabolic impact caused by their deficiencies have not been precisely characterized. To understand the systemic molecular alterations caused by peroxisomal defects, here we utilized untreated peroxisomal biogenesis factor 11α knockout (Pex11α KO) mouse model and performed serial relative-quantitative lipidomic, metabolomic, and proteomic analyses of serum, liver, and heart tissue homogenates. We demonstrated significant specific changes in the abundances of multiple lipid species, polar metabolites, and proteins and dysregulated metabolic pathways in distinct biological specimens of the Pex11α KO adult mice in comparison to the wild type (WT) controls. Overall, the present study reports comprehensive semi-quantitative molecular omics information of the Pex11α KO mice, which might serve in the future as a reference for a better understanding of the roles of Pex11α and underlying pathophysiological mechanisms of peroxisomal biogenesis disorders.
Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).
