Expression profiling of P14 and P28 mouse retina from 4 genotypes: +/+, Rorb-/- , +/+;CrxpNrl and Rorb-/-;CrxpNrl
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ABSTRACT: Rorb is essential for rod photoreceptor development in the mouse retina. Using Affymetrix mouse GeneChips, we have generated expression profiles of the +/+, Rorb-/- , +/+;CrxpNrl and Rorb-/-;CrxpNrl retina at P14 and P28. In this dataset, we include the expression data obtained from retina of wt and mutants. These data are used to obtain 1189 genes that are differentially expressed in Rorb-/- vs wt.
Project description:Rorb is essential for rod photoreceptor development in the mouse retina. Using Affymetrix mouse GeneChips, we have generated expression profiles of the +/+, Rorb-/- , +/+;CrxpNrl and Rorb-/-;CrxpNrl retina at P14 and P28. In this dataset, we include the expression data obtained from retina of wt and mutants. These data are used to obtain 1189 genes that are differentially expressed in Rorb-/- vs wt. Experiment Overall Design: 31 total samples were analyzed
Project description:To analyze the expression profile in the Mef2d KO retina, we performed a microarray analysis using wild-type and Mef2d KO retina at P14. We performed a microarray analysis using wild-type and Mef2d KO retina at P14, and compared the expression profiles.
Project description:To analyze the expression profile in the Mef2d KO retina, we performed a microarray analysis using wild-type and Mef2d KO retina at P14.
Project description:The PI3K/Akt signaling pathway impacts various aspects of CD8 T cell homeostasis, such as effect versus memory cell differentiation, during viral infection. We used microarrays to determine which downstream molecules were affected and what other signaling pathways were interconnected with the Akt pathway by constitutive activation of Akt in LCMV-infected CD8 T cells. Splenocytes from naive P14/WT or P14/Akt mice were stained with anti-CD8 and anti-Ly5.1, and CD8 T cells were sorted using a FACSAria II instrument. Purified Ly5.1+ CD8 T cells from P14/WT or P14/Akt mice were transferred into B6 mice, which were subsequently infected with LCMV Armstrong. At day 8 post infection, splenocytes were stained with anti-CD8, anti-Ly5.1, anti-KLRG1, and anti-CD127. Following staining, short-lived effector cells (SLECs) and memory precursor effector cells (MPECs) were sorted using the FACSAria II instrument; the purity of the sorted cells was >95%. A total of 5 samples were analyzed, including WT naive, WT SLEC, WT MPEC, Akt naive and Akt SLEC.
Project description:We used SLIC-CAGE to map transcriptional start sites (TSSs) of P14 WT and P14 Tbpl2-/- mutant mouse oocytes. Comparison of WT and Tbpl2-/- oocytes demonstrates that Tbpl2 guides transcriptional start site selection in the growing oocyte. This TSS selection is different compared to the canonical somatic type of TSS selection and depends on TATA-like elements as core promoter motifs, recognised by Tbpl2.
Project description:Osteoarthritis (OA) is the most prevalent chronic joint disease which increases in frequency with age eventually impacting most people over the age of 65. OA is the leading cause of disability and impaired mobility, yet the pathogenesis of OA remains unclear. Treatments have focused mainly on pain relief and reducing joint swelling. Currently there are no effective treatments to slow the progression of the disease and to prevent irreversible loss of cartilage. Here we demonstrate that stable expression of RORb in cultured cells results in alteration of a gene program that is supportive of chondrogenesis and is protective against development of OA. Specifically, we determined that RORb regulates the balance of FGFRs signaling on FGFR1/FGFR3 that ERK1/2-MAPK signaling was suppressed by FGFR1(cartilage destruction) and AKT signaling was enhanced by FGFR3 (cartilage protection). These results suggest a critical role for RORb in chondrogenesis and suggest that identification of mechanisms that control the expression of RORb in chondrocytes could lead to the development of disease modifying therapies for the treatment of OA