Project description:Histone deacetylase 3 (HDAC3) is a unique epigenetic regulator forming stoichiometric complexes with several other proteins. Patients with mutations in genes encoding these proteins display intellectual disability, implying an important role of HDAC3 in this prevalent disease. Here we report that cerebrum-specific inactivation of the mouse gene causes striking developmental defects in the neocortex, hippocampus and corpus callosum; post-weaning lethality; and abnormal behaviors, including hyperactivity and anxiety. The developmental defects are due to rapid loss of neural stem and progenitor cells (NSPCs), starting at E14.5. Premature neurogenesis and abnormal neuronal migration in the mutant brain alter NSPC homeostasis. Mutant cerebral cortices display augmented DNA damage, apoptosis, and histone hyperacetylation. In agreement with these results, mutant NSPCs are impaired in forming neurospheres in vitro, and treatment of wild-type NSPCs with the HDAC3-specific inhibitor RGFP966 abolishes neurosphere formation. Transcriptomic analyses of neonatal cerebral cortices and cultured neurospheres support that HDAC3 regulates various transcriptional programs through interaction with multiple transcription factors, including NFIB. These findings establish HDAC3 as a major deacetylase critical for perinatal development of the mouse cerebrum and NSPCs, thereby suggesting a direct link of this enzymatic epigenetic regulator to human cerebral and intellectual development. To study the impact of cerebrum specific (Emx1-Cre) deletion of Hdac3 on embryonic neurospheres (cultured in vitro from E16.5 cerebrum) and neocortex from newborn pups (P0).
Project description:We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2.
Project description:To determine the range of genes whose expression is regulated by CTDK-I under nitrogen starvation, comparison of gene expression profiles between a wild-type strain and a deletion mutant of lsg1, which encodes the gamma subunit of CTDK-I.
Project description:Transcriptome analysis of an LiAlba20 (LinJ.34.2410) null mutant strain versus Wild type. Experiments were run with promastigotes and axenic amastigotes independently. Null mutant was produced by homologous recombination, replacing both alleles with Hygromycin phosphotransferase and Puromycin.
Project description:We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2.
Project description:Three independent experiments: S. cervisiae wild-type (BY4741) and Puf3 mutant cells were grown in minimal medium supplemented with 3% glycerol. Cells were harvested in mid-log phase by centrifugation and total RNA was prepared by hot-phenol extraction. cDNA was prepared with oligo-dT and using a mixture of amino-allyl dUTP and dNTPs, fluorescently labeled (Cy3= wild-type, Cy5 = mutant) and hybridize on S. cerevisiae DNA microarray. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
Project description:ASF1 is a conserved histone chaperone with affinity to histone H3-H4. Arabidopsis thaliana genome encodes two ASF1 homologues, which play redundant roles in S-phase progression and cell proliferation in plant development. Here, in an attempt to obtain the knowledge of ASF1 role in transcriptional regulation, we perform the transcriptome analysis of each asf1 single mutant (Atasf1a and Atasf1b) as well as Atasf1ab double mutant in comparison with wild type (WT).
Project description:The goal of the study was to compare gene expression of P0 wild-type, P0 Fezf2-/- cortices, and Fezf2-/-; Fezf2-EnR cortices. Total RNAs were isolated from P0 cortices dissected from wild-type (n=3), Fezf2-/- mice (n=4), and Fezf2-/-; Fezf2-EnR cortices (n=2), following Qiagen RNAeasy kit instruction.Sequence libraries were made following Illumina RNA PolyA library preparation guide.The libaries were pair-end sequenced (150nt per end). Differentially expressed genes were identified by DESEQ.
Project description:Proteomes were compared between wild type Myxococcus xanthus (DK6204) and several mutant strains to determine relative changes in protein abundance when grown under normal conditions.