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Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells

ABSTRACT: Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells

PROVIDER: PRJNA107959 | ENA |

REPOSITORIES: ENA

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Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells.

Project description:We compared 12 different cell populations, including embryonic stem cells before and during differentiation into embryoid bodies as well as various types of normal and tumor cells to determine if pluripotent versus differentiated cell types use different mechanisms to establish their transcriptome. We first identified genes that were not expressed in the 12 different cell populations and then determined which of them were regulated by histone methylation, DNA methylation, at the step of productive elongation, or by the inability to establish a preinitiation complex. For these experiments, we performed chromatin immunoprecipitation using antibodies to H3me3K27, H3me3K9, 5-methyl-cytosine, and POLR2A. We found that (1) the percentage of low expressed genes bound by POLR2A, H3me3K27, H3me3K9, or 5-methyl-cytosine is similar in all 12 cell types, regardless of differentiation or neoplastic state; (2) a gene is generally repressed by only one mechanism; and (3) distinct classes of genes are repressed by certain mechanisms. We further characterized two transitioning cell populations, 3T3 cells progressing from G0/G1 into S phase and mES cells differentiating into embryoid bodies. We found that the transient regulation through the cell cycle was achieved predominantly by changes in the recruitment of the general transcriptional machinery or by post-POLR2A recruitment mechanisms. In contrast, changes in chromatin silencing were critical for the permanent changes in gene expression in cells undergoing differentiation.

| S-EPMC2279240 | biostudies-literature

Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells

Project description:We compared 12 different cell populations, including embryonic stem cells before and during differentiation into embryoid bodies as well as various types of normal and tumor cells to determine if pluripotent vs. differentiated cell types use different mechanisms to establish their transcriptome. We first identified genes that were not expressed in the 12 different cell populations and then determined which of them were regulated by histone methylation, DNA methylation, at the step of productive elongation, or by the inability to establish a pre-initiation complex. For these experiments, we performed chromatin immunoprecipitation using antibodies to H3me3K27, H3me3K9, 5-methyl cytosine, and POLR2A. We found that a) the percentage of low expressed genes bound by POLR2A, H3me3K27, H3me3K9, or 5-methyl-cytosine is similar in all 12 cell types, regardless of differentiation or neoplastic state; b) a gene is generally repressed by only one mechanism; and c) distinct classes of genes are repressed by certain mechanisms. We further characterized two transitioning cell populations, 3T3 cells progressing from G0/G1 into S phase and mES cells differentiating into embryoid bodies. We found that the transient regulation through the cell cycle was achieved predominantly by changes in the recruitment of the general transcriptional machinery or by post-POLR2A recruitment mechanisms. In contrast, changes in chromatin silencing were critical for the permanent changes in gene expression in cells undergoing differentiation. Keywords: ChIP-chip, RNA expression 48 ChIP-chip arrays; 12 expression arrays (6 of them in duplicates). 47 samples are included in this series, the rest can be found in supplementary info to the following papers: O'Geen 2007, Acevedo 2008, Acevedo 2007, Rinn 2007

2008-03-31 | E-GEOD-10504 | biostudies-arrayexpress

Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells

Project description:We compared 12 different cell populations, including embryonic stem cells before and during differentiation into embryoid bodies as well as various types of normal and tumor cells to determine if pluripotent vs. differentiated cell types use different mechanisms to establish their transcriptome. We first identified genes that were not expressed in the 12 different cell populations and then determined which of them were regulated by histone methylation, DNA methylation, at the step of productive elongation, or by the inability to establish a pre-initiation complex. For these experiments, we performed chromatin immunoprecipitation using antibodies to H3me3K27, H3me3K9, 5-methyl cytosine, and POLR2A. We found that a) the percentage of low expressed genes bound by POLR2A, H3me3K27, H3me3K9, or 5-methyl-cytosine is similar in all 12 cell types, regardless of differentiation or neoplastic state; b) a gene is generally repressed by only one mechanism; and c) distinct classes of genes are repressed by certain mechanisms. We further characterized two transitioning cell populations, 3T3 cells progressing from G0/G1 into S phase and mES cells differentiating into embryoid bodies. We found that the transient regulation through the cell cycle was achieved predominantly by changes in the recruitment of the general transcriptional machinery or by post-POLR2A recruitment mechanisms. In contrast, changes in chromatin silencing were critical for the permanent changes in gene expression in cells undergoing differentiation. Keywords: ChIP-chip, RNA expression

2008-03-31 | GSE10504 | GEO

Polycomb repression works without Siesta [ChIP]

Project description:Polycomb repression works without Siesta [ChIP]

| PRJNA1291712 | ENA

Macromolecular interactions dictate Polycomb-mediated epigenetic repression [ChIP-seq]

Project description:Macromolecular interactions dictate Polycomb-mediated epigenetic repression [ChIP-seq]

| PRJNA1133036 | ENA

Synthetic genomic reconstitution reveals principles of mammalian Hox cluster regulation [ChIP-Seq]

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| PRJNA788892 | ENA

Organoids-on-a-chip for Colorectal Cancer and in Vitro Screening of Chemotherapeutic Drugs

Project description:The individualized treatment of tumors has always been an urgent problem in clinical practice. Organoids-on-a-chip can reflect the heterogeneity of tumors and is a good model for in vitro anticancer drug screening. In this study, surgical specimens of patients with advanced colorectal cancer will be collected for organoid culture and organoids-on-a- chip. Use organoids-on-a-chip to screen tumor chemotherapy drugs, compare the results of patients’ actual medication regimens, and study the guiding role of organoids in the formulation of precise tumor treatment plans. The investigators will compare the response of organoids to drugs in vitro with the patient’s response to actual chemotherapy and targeted drugs and explore the feasibility and accuracy of organoids-on-a-chip based drug screening for advanced colorectal cancer. The project will establish a screening platform for chemotherapeutic drugs and targeted drugs based on colorectal cancer organoids to quickly and accurately formulate personalized treatment plans for clinical patients.

| 2385953 | ecrin-mdr-crc

Capturing totipotency in human cells through spliceosomal repression [ChIP-seq]

Project description:Capturing totipotency in human cells through spliceosomal repression [ChIP-seq]

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PR-DUB safeguards Polycomb repression through restricting H2AK119ub1 [ChIP-seq]

Project description:PR-DUB safeguards Polycomb repression through restricting H2AK119ub1 [ChIP-seq]

| PRJNA773660 | ENA

Vessel-on-a-Chip Coupled Proteomics Reveal Pressure-Overload-Induced Vascular Remodeling

Project description:We developed a vessel-on-a-chip to mimic both physiological and pathological stretch, along with a mouse model of hypertension. We applied proteomics analysis to investigate the changes in vascular smooth muscle cells using the vessel-on-a-chip system and changes in hypertensive mice.

2024-11-08 | PXD057724 |

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