Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)
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ABSTRACT: Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (RNA-seq)
Project description:This study characterized the genome-wide binding of histone 3 lysine 79 tri-methylation and expression profile of DOT1L knockdown in OVCAR5 cells.
Project description:This study characterized the genome-wide binding of histone 3 lysine 79 tri-methylation and expression profile of DOT1L knockdown in OVCAR5 cells.
Project description:Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells
Project description:Genome-wide maps of H3K79Me3 binding sites in ovarian cancer cell line OVCAR5 and expression profile of DOT1L knockdown OVCAR5 cells (ChIP-seq)
Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.
Project description:This study characterized the genome-wide binding of FOXK2 in ovarian cancer (OC) cell OVCAR-5 and investigated the expression profile of OVCAR5 cells with FOXK2 knocking-down.
Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.
Project description:Genome-wide maps of FOXK2 binding sites in ovarian cancer cell line OVCAR5 and expression profile of FOXK2 knockdown OVCAR5 cells (ChIP-seq)