Project description:We sequenced mRNA from three age groups (3months (3M), 24 months (24M) and 29 months (29M)) from the full hippocampus and compared this to microarray analysis. Young (3 months (3M)) mice were compared to aged mice (29 months (29M)), n=4
Project description:We sequenced mRNA from three age groups (3months (3M), 24 months (24M) and 29 months (29M)) from the full hippocampus There were two independent experiments: 3M vs 24M (n=5 to 6, single-end sequencing) and 3M vs 29M (n=3, paired-end sequencing))
Project description:The aim of the project was to determine the expression profiles of murine Myc-driven lymphpma cells (Lambda-820) treated with vehicle (DMSO, 1:1000), a BET inhibitor (RVX2135), an ATR inhibitor (VE-821) or a combination of RVX2135 and VE-821. All experimnets were performed in presence of 10uM Q-VD-OPH to block apoptosis. Cells were harvested 24 h after treatment start. 4 samples (DMSO, RVX2135, VE-821 or RVX2135/VE-821) in duplicates
Project description:We sequenced small RNAs from 12 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine miRNome under normal and Kat2a-loss-of-function conditions. Samples were divded in 4 groups: A: Control (n=6), C: Kat2a cKO naïve (n=6)
Project description:We sequenced mRNA from 24 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine transcriptome and the first CA1-transcriptome in response to environmental novelty under normal and Kat2a-loss-of-function conditions. Samples were divded in 4 groups: A: Control naM-CM-/ve (n=6), B: control novelty-exposed (n=5), C: Kat2a cKO naM-CM-/ve (n=6), D: Kat2a cKO novelty-exposed (n=7). Pairwise comparisons for AvsB, AvsC, BvsD and CvsD were performed using DESeq2.
Project description:Basal-like breast cancer generally shows a good response to conventional cytotoxic but rapidly develops a resistant phenotype. To better understand the epigenetic changes underlying the acquisition of resistant properties, we treated the murine basal-like mammary carcinoma cell line G-2 for 48 hours with sublethal combination chemotherapy (Cyclophosphamide, Adriamycin, 5-Fluorouracil) and subsequently subjected them to RNA- and ChIP-sequencing.
Project description:In mammalian cells, DNA methylation on the 5th position of cytosine (5mC) plays an important role as an epigenetic mark. However, DNA methylation was considered to be absent in C. elegans because of the lack of detectable 5mC as well as homologs of the cytosine DNA methyltransferases. Here, using multiple approaches, we demonstrate the presence of adenine N6-methylation (6mA) in C. elegans DNA. We further demonstrate that this modification increases trans-generationally in a paradigm of epigenetic inheritance. Importantly, we identify a DNA demethylase, NMAD-1, and a potential DNA methyltransferase, DAMT-1, which regulate 6mA levels and crosstalk between methylation of histone H3K4me2 and 6mA, and control the epigenetic inheritance of phenotypes associated with the loss of the H3K4me2 demethylase spr-5. Together, these data identify a novel DNA modification in C. elegans and raise the exciting possibility that 6mA may be a carrier of heritable epigenetic information in eukaryotes. SMRT-sequencing for a mixed cell population of wildtype worms 6mA ChIP-Seq for a mixed cell population of wildtype worms
Project description:The goal of this study is to determine the effects of adipose-specific Glut4 overexpression or knockout on changes in adipose tissue global gene expression Three mice from each of four genotypes were studied using a total of 12 microarray chips: aP2-Cre transgenic mice (controls for adipose-Glut4-/- mice), adipose-Glut4-/- mice; FVB mice (littermate controls for adipose-GLUT4-Tg mice) and adipose-GLUT4-Tg mice with Glut4 transgenically overexpressed under the control of the aP2 promoter. Total RNA from perigonadal adipose tissue was extracted using the RNeasy Mini Kit from Qiagen. Affymetrix gene chip hybridization and analysis were performed at the Genomics Core Facility of the Beth Israel Deaconess Medical Center.
Project description:Gene expression studies were performed to identify pathways possibly dysregulated by mutant in the gene GM-NM-1(olf). These experiments employed RNA derived from lymphoblastoid cell lines established for 4 affected carriers and 4 non-carriers. In comparison to endogenous control and other dystonia-associated genes, GNAL was expressed at relatively low levels in lymphoblastoid cell lines. Comparison of whole blood expression profiles of mutation carrying dystonia patients with normal controls