Project description:Transcription profiling by array of wild type and p300 KIX/KIX; CBP +/KIX primary mouse embryonic fibroblasts (MEFs) transduced with either MSCV-c-Myb_IRES-GFP or MSCV-IRES-GFP retrovirus to determine the effect of mutating the KIX domain of CBP and p300 on c-Myb regulated gene expression. CBP KIX mutation (MGI:3578129) and p300 KIX mutation (MGI:3578128).
Project description:Dmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. This study examines the result of conditional removal of Dmrt1 from Sertoli cells in P28 testis tissue. Testes from P28 Dmrt1 flox/flox mice were compared to testes from P28 Dmrt1 flox/flox mice with the Sertoli cell-specific Sf1 (Nr5a1; MGI:1346833) or Dhh (MGI:94891) promoters driving Cre expression.
Project description:Three congenic mouse strains were profiled with microarrays and were analyzed using a QTL/Microarray approach to identify candidate genes that regulate biometric phenotypes: HG2D (HG.CAST-(D2Mit329-D2Mit457)), HG11 (HG.CAST-(D11Mit260-D11Mit255, MGI reference: 3771218), and HG17 (HG.CAST-(D17Mit196-D17Mit190); MGI reference: 3771215). All these congenic strains isolate CAST/EiJ (CAST) alleles in a C57BL/6Jhg/hg (C57) background and bare the hg deletion in the high growth locus on chromosome 10. F2 animals from intercrossing congenic males and C57 control females were profiled for gene expresion on brain, liver and gonadal white fat. To detect differential expression produced by allelic effects of biometric QTLs on chromosomes 2, 11, and 17.
Project description:Three congenic mouse strains were profiled with microarrays and were analyzed using a QTL/Microarray approach to identify candidate genes that regulate biometric phenotypes: HG2D (HG.CAST-(D2Mit329-D2Mit457)), HG11 (HG.CAST-(D11Mit260-D11Mit255, MGI reference: 3771218), and HG17 (HG.CAST-(D17Mit196-D17Mit190); MGI reference: 3771215). All these congenic strains isolate CAST/EiJ (CAST) alleles in a C57BL/6Jhg/hg (C57) background and bare the hg deletion in the high growth locus on chromosome 10. F2 animals from intercrossing congenic males and C57 control females were profiled for gene expresion on brain, liver and gonadal white fat. To detect differential expression produced by allelic effects of biometric QTLs on chromosomes 2, 11, and 17. Three strains were profiled: HG2D, HG11, and HG17, isolating CAST alleles in a high growth (HG) background on chromosomes 2, 11, and 17 respectively. Four biological replicates were assayed per strain for brain, liver and gonadal white adipose tissue. Experiments for each chromosomes were done independently. Only genotype comparisons within tissue in each strain were performed.
Project description:The observation that Tcf3 (MGI name: Tcf7l1) bound the same genes as core stem cell transcription factors, Oct4 (MGI name:Pou5f1), Sox2 and Nanog, revealed a potentially important aspect of the poorly understood mechanism whereby Wnts stimulate self renewal of pluripotent mouse embryonic stem (ES) cells. Although the conventional view of Tcf proteins as the β-catenin-binding effectors of Wnt signaling suggested Tcf3 should activate target genes in response to Wnts, here we show that Wnt3a and Tcf3 effectively antagonize each other’s effects on gene expression. Genetic ablation of Tcf3 caused similar effects as treating cells with recombinant Wnt3a. Moreover, Tcf3 was not necessary for Wnt3a-stimulation of gene expression as the majority of Wnt3a-stimulated genes exhibited a greater increase in Tcf3-/- ES cells than in Tcf3+/+ ES cells. These expression data, together with genetic experiments, show that Wnt3a stimulates ES cell self renewal by inhibiting Tcf3.
Project description:The observation that Tcf3 (MGI name: Tcf7l1) bound the same genes as core stem cell transcription factors, Oct4 (MGI name:Pou5f1), Sox2 and Nanog, revealed a potentially important aspect of the poorly understood mechanism whereby Wnts stimulate self renewal of pluripotent mouse embryonic stem (ES) cells. Although the conventional view of Tcf proteins as the β-catenin-binding effectors of Wnt signaling suggested Tcf3 should activate target genes in response to Wnts, here we show that Wnt3a and Tcf3 effectively antagonize each other’s effects on gene expression. Genetic ablation of Tcf3 caused similar effects as treating cells with recombinant Wnt3a. Moreover, Tcf3 was not necessary for Wnt3a-stimulation of gene expression as the majority of Wnt3a-stimulated genes exhibited a greater increase in Tcf3-/- ES cells than in Tcf3+/+ ES cells. These expression data, together with genetic experiments, show that Wnt3a stimulates ES cell self renewal by inhibiting Tcf3. Tcf3+/+ and Tcf3-/- mouse embryonic stem cells were cultured in self renewal conditions containing recombinant Wnt3a for RNA extraction and hybridization on Affymetrix microarrays.
Project description:To investigate the impact of Stxbp6 knockout on the brain, we carried out transcriptome analysis on the cortexes of Stxbp6-null (n = 3, KO) and wildtype mice (n = 3, WT) and identified 126 differentially expressed genes (DEGs) in the KO group, of which 57 were upregulated and 69 were downregulated. RNA-seq was performed on the BGISEQ platform by MGI Technology Co., Ltd, Guangdong, China.