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Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [K562]

ABSTRACT: Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [K562]

PROVIDER: PRJNA541309 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9019504_1.fastq.gz	Fastqsanger.gz
	SRR9019504_2.fastq.gz	Fastqsanger.gz
	SRR9019505_1.fastq.gz	Fastqsanger.gz
	SRR9019505_2.fastq.gz	Fastqsanger.gz
	SRR9019506_1.fastq.gz	Fastqsanger.gz

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Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [K562]

Project description:Heat shock (HS) causes dramatic and rapid changes in transcription of thousands of genes in metazoans. We have used insitu Hi-C in Drosophila S2 and human K562 cells to determine the effects of HS upon chromatin conformation. Our study shows that topologically associated domains (TADs), compartments and distal regulatory interactions remain unchanged upon HS.

2019-06-07 | GSE130758 | GEO

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock

Project description:Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock

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Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [S2]

Project description:Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [S2]

| PRJNA541321 | ENA

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [S2]

2019-06-07 | GSE130776 | GEO

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock.

Project description:Heat shock (HS) initiates rapid, extensive, and evolutionarily conserved changes in transcription that are accompanied by chromatin decondensation and nucleosome loss at HS loci. Here we have employed in situ Hi-C to determine how heat stress affects long-range chromatin conformation in human and Drosophila cells. We found that compartments and topologically associating domains (TADs) remain unchanged by an acute HS. Knockdown of Heat Shock Factor 1 (HSF1), the master transcriptional regulator of the HS response, identified HSF1-dependent genes and revealed that up-regulation is often mediated by distal HSF1 bound enhancers. HSF1-dependent genes were usually found in the same TAD as the nearest HSF1 binding site. Although most interactions between HSF1 binding sites and target promoters were established in the nonheat shock (NHS) condition, a subset increased contact frequency following HS. Integrating information about HSF1 binding strength, RNA polymerase abundance at the HSF1 bound sites (putative enhancers), and contact frequency with a target promoter accurately predicted which up-regulated genes were direct targets of HSF1 during HS. Our results suggest that the chromatin conformation necessary for a robust HS response is preestablished in NHS cells of diverse metazoan species.

| S-EPMC6765289 | biostudies-literature

Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-07 | GSE130778 | GEO

Chromatin Conformation Capture in two biological replicates of K562 cells to identify interactions between tRNA genes in human cells.

Project description:tRNA genes are believed to form clusters in three-dimensional space in smaller eukaryotes (yeasts). In the course of investigating a cluster of tRNA genes for insulator activity in humans, we addressed whether these tRNA genes clustered with other tRNA genes. We used an anchor point to generate 4C material from a tRNA cluster located on chromosome 17 (hg18 7.962400 MB). We identify interactions occurring within the 300kb region of this point, but only extending in one direction and suggesting these interactions occur between this tRNA cluster and other tRNA gene clusters from this locus. We did not observed any specific interactions outside of this region or on other chromsomes, perhaps due to an low number of mappable reads from our samples. Chromatin Conformation Capture in two biological replicates of K562 cells to identify interactions between tRNA genes in human cells.

2011-10-10 | E-GEOD-31105 | biostudies-arrayexpress

RNA-seq analysis of K562 cells (K562-shX) with stable integration of a tet-inducible shRNA targeting a candidate (X) transcription factor from ENCODE/HudsonAlpha-MyersLab

Project description:K562-shX cells are made in an effort to validate TFBS data and ChIP-seq antibodies in Myers lab (GSE32465). K562 cells are transduced with lentiviral vector having Tet-inducible shRNA targeting a transcription factor gene. Cells with stable integration of shRNA constructs are selected using puromycin in growth media. Doxycycline is added to the growth media to induce the expression of shRNA and a red fluorescent protein marker. A successful shRNA cell line shows at least a 70% reduction in expression of the target transcription factor as measured by qPCR. For identification, we designated these cell lines as K562-shX, where X is the transcription factor targeted by shRNA and K562 denotes the parent cell line. For example, K562-shATF3 cells are K562 derived cells selected for stable integration of shRNA targeting the transcription factor ATF3 gene and showed at least a 70% reduction in the expression of ATF3 gene when measured by qPCR. Cells growing without doxycycline (uninduced) are used as a control to measure the change in expression of target transcription factor gene after induction of shRNA using doxycycline. For detailed growth and culturing protocols for these cells please refer to http://hudsonalpha.org/sites/default/files/pdf/shRNA%20K562%20protocol.pdf. To identify the potential downstream targets of the candidate transcription factor, analyze the mRNA expression profile of the uninduced and induced K562-shX using RNA-seq. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Make K562-shX cells as described in the http://hudsonalpha.org/sites/default/files/pdf/shRNA%20K562%20protocol.pdf. Measure the mRNA expression levels in uninduced K562-shX and induced K562-shX cells in two biological replicates using RNA-seq. Identify the potential downstream targets of the candidate transcription factor.

2011-12-01 | E-GEOD-33816 | biostudies-arrayexpress

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