Project description:Microarray analysis of gene expression in the olfactory epithelium of Harlequin mouse as a model of oxidative-stress induced neurodegeneration of olfactory sensory neurons Experiment Overall Design: Olfactory epithelium from Harlequin mutant mice and littermate control mice was microdissected for RNA extraction and hybridization on Affymetrix microarrays. We compared levels of gene expression in 6-month old mice to begin to identify mechanisms of oxidative-stress induced neurodegeneration and to correlate the cellular changes that we observed in the olfactory epithelium by using histology and immunohistochemistry with gene expression changes.
Project description:Microarray analysis of gene expression in the olfactory epithelium of Harlequin mouse as a model of oxidative-stress induced neurodegeneration of olfactory sensory neurons Keywords: comparison of gene expression level in unperturbed tissue of mutant vs. control mouse
Project description:Purpose: To asses changes in gene expression profiles from the P11 no cre littermate control olfactory bulbs and conditional double knockout olfactory bulbs of Dlx5/6-CIE; Sp8 Flox/Flox; Sp9 Flox/Flox (Sp8/Sp9-DCKO) mice. Methods: Total RNA was isolated and sequenced from the olfactory bulbs of the P11 no cre littermate controls or Sp8/Sp9-DCKO mice in duplicate using an illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered changed which performed fold-change>=2 and FDR<=0.05. Changed genes were then filtered to reveal the downstream targets of Sp8 and Sp9. Results: 32 genes were significantly increased and 144 genes were significantly decreased in expression level due to the loss of Sp9 and Sp8 expression.
Project description:Purpose: To asses changes in gene expression profiles from the P30 wild type littermate control olfactory bulbs and conditional double knockout olfactory bulbs of hGFAP-Cre; Sp8 Flox/Flox; Sp9 Flox/Flox mice. Methods: Total RNA was isolated and sequenced from the olfactory bulbs of the P30 wild type littermate controls or hGFAP-Cre; Sp8 Flox/Flox; Sp9 Flox/Flox mice in tetrad using an illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered changed which performed fold-change>=2 and FDR<=0.05. Changed genes were then filtered to reveal the downstream targets of Sp8 and Sp9. Results: 31 genes were significantly increased and 74 genes were significantly decreased in expression level due to the loss of Sp9 and Sp8 expression.
Project description:Purpose:To asses changes in gene expression profiles of cortices from the P0 wild type littermate controls and Tle4-/- null mutant mice. Methords:Total RNA was isolated and sequenced using an illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed whicn perform P value <= 0.05 Results: Compared to controls, 306 genes were significantly down-regulated in the Tle4 null mutant mice, and 338 genes were significantly up-regulated in the Tle4 null mutant mice.
Project description:Transcriptional profiles were compared in microdissected lateral walls of the inner ears from Errb mutant mice and wild type littermate controls. The goal is to identify transcriptional targets of Errb and candidate genes for inner ear diseases. Keywords: genetic mutant analysis
Project description:RNA sequencing for differential gene expression analysis was performed from brain and muscle of Nadk2 mutant mice and littermate controls at 5 and 11 weeks of age, and in Pla2g6 mutant mice and littermate controls at 6 and 13 weeks of age, representing early stage and late stage phenotypic time points.
Project description:Dr. Schwarting's research is focused on the analysis of developmentally regulated cell surface molecules and their role in axon guidance and neuronal migration, using the olfactory system as a model. The interaction of cell surface glycans with endogenous lectins in the extracellular matrix provides one mechanism by which axons can utilize specific pathways as they grow towards their targets. Beta3GnT1 mutant mice lose lactosamine expression and have an olfactory axon guidance phenotype (Henion et al, 2005). Olfactory neurons are capable of regeneration and we know that when these neurons regenerate in beta3GnT1 mutant they synthesize lactosamine by a secondary mechanism. By comparing RNA from the olfactory epithelium from wild type and mutant mice, we would expect to see the upregulation of glycosyltransferases that could produce lactosamine in the absence of beta3GnT1. In a preliminary experiment carried out by the CFG staff, we saw that radical fringe, a beta 3GnT, was upregulated in the olfactory epithelium, although it is probably not responsible for the new lactosamine expression. beta3GnT1 Knock out. Strain info: The b3GnT1 mice were generated on a mixed 129Ola-C57BL/6 background and backcrossed to C57BL/6 for four generations. They were then crossed to I7-Internal ribosomal entry site (IRES)-tau greeen fluorescent protein (GFP) mice generated by Dr. Peter Mombaerts. RNA preparations from wild type and beta3GnT1 mutant mouse olfactory epithelium were sent to Microarray Core (E). Three replicate samples from each condition were used in the study. The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays. Data was analyzed to determine glycosyltransferase expression changes in beta3GnT1 mutant mice, with specific interest on glycosyltransferases that could produce lactosamine in the in the absence of beta3GnT1.
