Project description:Transcriptional profiling of normal human diploid fibroblasts(TIG-3) infected with retrovirous encoding DP1-shRNA or control-shRNA.
Project description:Transcriptional profiling of normal human diploid fibroblasts(TIG-3) infected with retrovirous encoding DP1-shRNA or control-shRNA. TIG-3 cells were subjected to infection with retrovirus encoding DP1-shRNA or control-shRNA. Total RNA was isolated using TRIzol reagent and were analyzed using the human 3D-Gene DNA chip (Toray) that contains 25000 genes. The genome wide transcriptional
Project description:Here we report the identification of genomic regions of DNA bound by Dp1 in Drosophila S2R+ cells. Dp1 is a dimerization partner of several E2F transcription factors and is needed for E2F target promoter binding. We find that Dp1 binds the promoter regions of genes important for oxidative phosphorylation. This result is important since our data demonstrates that expression of several oxidative phosphorylation genes is down-regulated in dDP mutant Drosophila 3rd instar larval eye imaginal discs. These ChIP-seq results suggest that the mechanism by which dDP regulates expression of these genes is direct. In addition, we have confirmed a number of these Dp1 bound gene promoters by conventional Chromatin Immunoprecipitation. Examination of Dp1 bound regions of genomic DNA in S2R+ cells.
Project description:Here we report the identification of genomic regions of DNA bound by Dp1 in Drosophila S2R+ cells. Dp1 is a dimerization partner of several E2F transcription factors and is needed for E2F target promoter binding. We find that Dp1 binds the promoter regions of genes important for oxidative phosphorylation. This result is important since our data demonstrates that expression of several oxidative phosphorylation genes is down-regulated in dDP mutant Drosophila 3rd instar larval eye imaginal discs. These ChIP-seq results suggest that the mechanism by which dDP regulates expression of these genes is direct. In addition, we have confirmed a number of these Dp1 bound gene promoters by conventional Chromatin Immunoprecipitation.
Project description:The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes, and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or premRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation. Keywords: MALAT1; MALAT-1, NEAT2, ncRNA; E2F, alternative splicing; pre-mRNA splicing factors WI38 cells (normal human diploid fibroblasts) were transfected with a control oligo (CTR) or antisense oligos to MALAT1 and RNA was isolated after 48 hr. Two antisense oligos were use for MALAT1 (AS-1 and AS-2). Arrays were done for 3 sets of samples in triplicate (control, AS-1 and AS-2).