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ChIPseq on H3K27ac, H4ac, H3K9ac, H3K4me3, H3K4me1, H3K27me3 and H2AK119Ub on TX1072 WT, Hdac3-/-, and ChIP targeting FLAG on Hdac3-AID-FLAG cell lines, at different time of Dox induction.

ABSTRACT: ChIPseq on H3K27ac, H4ac, H3K9ac, H3K4me3, H3K4me1, H3K27me3 and H2AK119Ub on TX1072 WT, Hdac3-/-, and ChIP targeting FLAG on Hdac3-AID-FLAG cell lines, at different time of Dox induction.

PROVIDER: PRJNA480803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7514300_1.fastq.gz	Fastqsanger.gz
	SRR7514300_2.fastq.gz	Fastqsanger.gz
	SRR7514310_1.fastq.gz	Fastqsanger.gz
	SRR7514310_2.fastq.gz	Fastqsanger.gz
	SRR7514320_1.fastq.gz	Fastqsanger.gz

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ChIPseq on H3K27ac, H4ac, H3K9ac, H3K4me3, H3K4me1, H3K27me3 and H2AK119Ub on TX1072 WT, Hdac3-/-, and ChIP targeting FLAG on Hdac3-AID-FLAG cell lines, at different time of Dox induction.

Project description:During development, transcriptional and chromatin modification changes co-occur but the order and causality of events often remain unclear. We explore these questions using the paradigm of X-chromosome inactivation (XCI). We initiate XCI in female, mouse embryonic stem cells by inducingXistand monitor changes in transcription and chromatin by allele-specific profiling. Our unprecedented temporal resolution identifies histone deacetylation and H2AK119 ubiquitination as the earliest chromatin alterations during XCI. Functional dissection of these changes reveals that HDAC3 is pre-bound on the X-chromosome and uponXistcoating, histone deacetylation is required for efficient gene silencing. We also reveal that PRC1-associated H2AK119Ub precedes PRC2-associated H3K27me3 during XCI. These marks accumulate initially at large, intergenic domains and then spread into genes but only in the context of gene silencing and histone deacetylation. Our results reveal a hierarchy of chromatin events at the initiation of XCI and identify their key roles in mediating transcriptional silencing.

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TTseq on TX1072 during time course of DOX induction

Project description:During development, changes in gene transcription are accompanied by changes in chromatin modification but the order and causality of events often remain unclear. Here we address this question using X-chromosome inactivation (XCI), which entails chromosome-wide gene silencing and heterochromatin formation. We initiate XCI in female, mouse embryonic stem cells by inducing Xist expression and monitor subsequent changes in transcription and chromatin modification by allele-specific TTseq and ChIPseq respectively. An unprecedented temporal resolution has enabled us to define early alterations in chromatin that are induced upon Xist RNA coating. Xist-induced repression begins with histone deacetylation, which involves the histone deacetylase HDAC3 and occurs before efficient loss of H3K4me3 and H3K4me1 modifications. Polycomb-associated repressive histone marks accumulate rapidly, starting with PRC1-associated H2AK119Ub and followed by PRC2-associated H3K27me3. However, polycomb accumulates initially at large premarked domains, some of which correspond to Xist entry sites, and then spreads into genes. We also show that spreading can only ensue when transcriptional silencing has occurred. These results establish a detailed epigenomic time course for XCI and reveal a hierarchy of events with chromatin playing an important role in transcriptional silencing of the X chromosome.

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Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

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TTseq on TX1072 during time course of DOX induction

Project description:TTseq on TX1072 during time course of DOX induction

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CUT&Tag on H3K4me3, H3K27ac, H3K4me1, H3K9me3, H3K27me3, H3K36me3 and H2AK119ub in TX1072 XXΔXic and XO mESCs during differentiation

Project description:CUT&Tag on H3K4me3, H3K27ac, H3K4me1, H3K9me3, H3K27me3, H3K36me3 and H2AK119ub in TX1072 XXΔXic and XO mESCs during differentiation

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HDAC3 preferentially binds to RUNX1 in t(8;21) AML cells and collaborates with RUNX1 to repress AML1-ETO-mediated transcriptional activation

Project description:Human histone deacetylase 3 (HDAC3) plays an important role in gene transcription in diseased human cells, such as leukemia. The t(8;21) chromosomal translocation is one of the most commonly observed genetic abnormalities associated with acute myeloid leukemia. This translocation generates the AML1-ETO fusion protein between the wild-type RUNX1 transcription factor and wild-type ETO transcriptional corepressor. To better understand the role of HDAC3 in t(8;21) leukemogenesis, the human HDAC3-containing complexes were isolated from stably-transfected HeLa cells by using anti-FLAG immunoprecipitation. The resulting complexes were resolved in SDS-PAGE. The components of the complexes were identified using LC-MS/MS. We report here that the human RUNX1 transcription is a component of the HDAC3 complexes. We demonstrate that HDAC3 and RUNX1 collaboratively repress AML1-ETO-mediated transcription. These results reveal new insight into how AML1-ETO, RUNX1, and HDAC3 crosstalk to deregulate gene transcription in t(8;21) leukemia cells.

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RNAseq in Dppa2 knockout or wildtype TX1072 ESC during and after Xist over-expression

Project description:To understand the role of DPPA2 in epigenetic memory during X-Chromosome reactivation (XCR) we employed inducible Xist hybrid female embryonic stem cell line (TX1072, hybrid Bl6/Cast). Wild type or Dppa2 knockout TX1072 cells were cultured, in three or two independent biological replicates, respectively, in presence of DOX (1ug/ml) for 6 days to induce Xist overexpression and X-Chomosome inactivation (XCI) on the Bl6 allele. DOX was then washed out to silence Xist and XCR was followed in a time-series at 1, 3 or 7 days after DOX removal. Cell pellets were harvested at the following timepoints: -DOX, +DOX, 1d D-wo, 3d D-wo and 7d D-wo. RNA was extracted and 250 ng used for PolyA mRNA library preparation and Next generation sequencing.

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