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Nucleosome accessibility in CUTLL3 cell line treated with Vehicle or Pitavastatin and 3 ETP-ALL patients

ABSTRACT: Nucleosome accessibility in CUTLL3 cell line treated with Vehicle or Pitavastatin and 3 ETP-ALL patients

PROVIDER: PRJNA692468 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13444339_1.fastq.gz	Fastqsanger.gz
	SRR13444339_2.fastq.gz	Fastqsanger.gz
	SRR13444340_1.fastq.gz	Fastqsanger.gz
	SRR13444340_2.fastq.gz	Fastqsanger.gz

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Nucleosome accessibility in CUTLL3 cell line treated with Vehicle or Pitavastatin and 3 ETP-ALL patients

Project description:Analysis of nucleosome accessibility in CUTLL3 ETP-ALL cells following treatment with Vehicle or Pitavastatin for 48 hours and ETP-ALL patients at diagnosis

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H3K27acetylation ChIP-seq in CUTLL3 cell line treated with Vehicle or Pitavastatin

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RNA-seq in CUTLL3 cell line treated with Vehicle or Pitavastatin

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RNA-seq in CUTLL3 cell line treated with Vehicle or Pitavastatin

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H3K27acetylation ChIP-seq in CUTLL3 cell line treated with Vehicle or Pitavastatin

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Combined pitavastatin and capmatinib inhibits tumor growth though completed shutdown of MET signal

Project description:To reveal the function of pitavastatin in cancer, we performed several experiments. In the present study, we show that pitavastatin inhibits the tumor growth through the inactivation of ERK and AKT signals by MET immaturation, and combination of pitavastatin and capmatinib, a MET inhibitor, might be useful cancer therapy in OSCC and ESCC. It could be reduced the dose of pitavastatin by using this combination therapy, resulting in decreasing the risk of adverse events such as myopathy. Taken together, the mevalonate pathway regulates the processes of MET maturation and promotes the cell growth in cancer. Moreover, the expression of GGPS1, an enzyme that synthesizes geranylgeranyl pyrophosphate (GGPP) from farnesyl pyrophosphate (FPP), associates with the sensitivity of pitavastatin, suggesting that GGPS1 could be a biomarker in cancer therapy with pitavastatin. Identification of the function of pitavastatin in oral and esophageal squamous cell carcinoma.

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MNase titration reveals differences between nucleosome occupancy and chromatin accessibility

Project description:Chromatin accessibility plays a fundamental role in gene regulation. One mechanism to regulate accessibility is nucleosome placement, which is often measured by quantifying protection of DNA from enzymatic digestion. We introduce a metric that uses micrococcal nuclease (MNase) digestion in a novel manner to measure chromatin accessibility by combining information from several digests of increasing depths. This metric, MACC, quantifies the inherent heterogeneity of nucleosome accessibility in which some nucleosomes are seen preferentially at high MNase and some at low MNase. MACC interrogates each genomic locus, measuring both location of nucleosomes and accessibility to MNase in the same assay. MACC can be performed either with or without a histone immunoprecipitation step, and thereby compares behavior of nucleosomes to that of non-histone proteins. We find that enhancers, promoters and other regulatory regions have changes in accessibility that do not correlate with changes in nucleosome occupancy. Moreover, we show that high nucleosome occupancy does not necessarily preclude high accessibility, revealing novel principles of chromatin regulation.

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Project description:Activation of transcription requires alteration of chromatin by complexes that increase the accessibility of nucleosomal DNA. Removing nucleosomes from regulatory sequences has been proposed to play a significant role in activation. We tested whether changes in nucleosome occupancy occurred on the set of genes that are activated by the unfolded protein response (UPR). We observed no decrease in occupancy on most promoters, gene bodies, and enhancers. Instead there was an increase in the accessibility of nucleosomes, as measured by MNase digestion and by ATAC-seq, that did not result from removal of the nucleosome. Thus changes in nucleosome accessibility predominate over changes in nucleosome occupancy during rapid transcriptional induction during the UPR.

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mRNA expression profile in HeLa cells that subject to pitavastatin treantment.

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Project description:Nucleosome positioning is critical to chromatin accessibility, and is associated with gene expression programs in cells. Previous nucleosome mapping methods assemble profiles from cell populations and reveal a cell-averaged pattern: nucleosomes are positioned and form a phased array surrounding the transcription start sites (TSSs ) of active genes and DNase I hypersensitive sites (DHSs). However, cells exhibit remarkable expression heterogeneity in response to active signaling even in a homogenous population of cells, which may be related to the heterogeneity in chromatin accessibility. Here, we report a technique, termed single-cell MNase-seq (scMNase-seq), to measure genome-wide nucleosome positioning and chromatin accessibility simultaneously in single cells. Application of scMNase-seq to NIH3T3, mouse primary naïve CD4 T and embryonic stem cells (mESC) reveals two novel principles of nucleosome organization: (1) nucleosomes surrounding TSSs of silent genes or in heterochromatin regions show large positioning variation across different cells but are highly uniformly spaced along the nucleosome array and, (2) In contrast, nucleosomes surrounding TSSs of active genes and DHSs show small positioning variation across different cells but show relatively low spacing uniformness along the nucleosome array. We found a bimodal distribution of nucleosome spacing at DHSs, which corresponds to inaccessible and accessible states and is associated with nucleosome variation and accessibility variation across cells. Nucleosome variation within single cells is smaller than that across cells and variation within the same cell type is smaller than that across cell types. A large fraction of naïve CD4 T cells and mESCs show depleted nucleosome occupancy at the de novo enhancers detected in their respectively differentiated lineages, revealing the existence of cells primed for differentiation to specific lineages in undifferentiated cell populations.

2018-07-23 | GSE96688 | GEO

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