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Expression data from control and heat shocked mouse spermatocytes and hepatocytes

ABSTRACT: In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide transcriptional analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results. Genes that are differently regulated during hyperthermia in both types of cells have been identified.

ORGANISM(S): Mus musculus

PROVIDER: GSE40248 | GEO | 2012/08/22

SECONDARY ACCESSION(S): PRJNA173340

REPOSITORIES: GEO

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Expression data from control and heat shocked mouse spermatocytes and hepatocytes

Project description:In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide transcriptional analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results. Genes that are differently regulated during hyperthermia in both types of cells have been identified. On Affymetrix gene chip arrays we analyzed RNA isolated from spermatocytes or hepatocytes, either untreated (control) or after heat shock and 2h of recovery at physiological temperature. Analyses were done in triplicate.

2012-08-22 | E-GEOD-40248 | biostudies-arrayexpress

Genome-wide HSF1 binding sites in control and heat shocked spermatocytes and hepatocytes

Project description:In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To find out molecular targets of HSF1 in all promoter regions, and to elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide HSF1 binding analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results. On Affymetrix GeneChipM-BM-. Mouse Promoter 1.0R Arrays we analyzed DNA immunoprecipitated (using anty-HSF1 antibody) from spermatocytes or hepatocytes, either untreated (control) or immediately after heat shock performed in vitro for 5-20 minutes. ChIP on chip analyses were done in triplicate.

2012-08-28 | E-GEOD-40390 | biostudies-arrayexpress

Genome-wide HSF1 binding sites in control and heat shocked spermatocytes and hepatocytes

Project description:In somatic cells elevated temperature induces activation of the heat shock transcription factor 1 (HSF1) what leads to heat shock proteins synthesis and cytoprotection. However, in the male germ cells (spermatocytes) upon HSF1 activation, caspase-3 dependent apoptosis is induced and spermatogenic cells are actively eliminated. To find out molecular targets of HSF1 in all promoter regions, and to elucidate a mechanism of such diverse HSF1 activity we carried out genome-wide HSF1 binding analysis in control and heat-shocked cells, either spermatogenic or somatic. As model somatic cells we used hepatocytes that respond to hyperthermia in a classical way by induction of heat shock genes transcription. As spermatogenic cells we used a fraction of cells enriched with spermatocytes, which are the most sensitive to damage in elevated temperatures. Using isolated spermatocytes we avoided the influence of the somatic testicular component on the our final results.

2012-08-28 | GSE40390 | GEO

HSF1 and HSF2 interactions with chromatin during the heat shock response in mouse spermatocytes

Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43M-BM-0C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38M-BM-0C. In contrary at 43M-BM-0C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38M-BM-0C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock. On Illumina platform we sequenced DNA immunoprecipitated from isolated spermatocytes using anti-HSF1 antibody or anti-HSF2 antibody. Cells were either untreated (control) or heat shocked for 5-20 minutes. Two PCR-verified ChIP replicates were collected per each sample, and three negative control samples with normal goat serum were included.

2014-10-07 | E-GEOD-56735 | biostudies-arrayexpress

HSF1 and HSF2 interactions with chromatin during the heat shock response in mouse spermatocytes

Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43°C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38°C. In contrary at 43°C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38°C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock.

2014-10-07 | GSE56735 | GEO

Expression data from 15-day-old mouse testes

Project description:Activation of the Heat Shock Factor 1 (HSF1) in spermatogenic cells leads to apoptosis and infertility of males. To elucidate a mechanisms of apoptosis induced by HSF1 we generated transgenic mice expressing mutated, constitutively active human HSF1 (with a deletion of amino acids 221–315) specifically in spermatocytes (under control of the rat Hspa2 promoter). We carried out genome-wide transcriptional analyses in testes of control, wild-type, and transgenic males. Genes that changed the expression due to activation of HSF1 have been identified.

2019-03-29 | GSE128996 | GEO

Subsets of NFkappaB-dependent genes are differentially regulated after combined treatment with hyperthermia and cytokine

Project description:Heat shock transcription factor 1 (HSF1) is responsible for triggering stress-induced activation of the HSP genes. HSF1 is also involved in the regulation of many other genes associated with multiple cellular processes including cell signaling, development, fertility, cell death and metabolism, e.g. NFkappaB transcription factor. Here we aimed to establish a global picture for the association between hyperthermia-modulated expression of NFkappaB-dependent genes and HSF1 binding in regulatory regions of target genes. The global pattern of HSF1 binding was analyzed after 10 and 20 minutes of hyperthermia using the ChIP-Seq approach. The analysis revealed about 25,000 HSF1 binding sites in chromatin of control untreated U-2 OS cells, which nearly doubled in cells subjected to hyperthermia. The presence of hyperthermia-induced HSF1 binding was established in regulatory regions of hyperthermia-affected genes and in TNF-affected genes. In most cases hyperthermia pre-conditioning inhibited cytokine-mediated activation of NF-?B-dependent genes. However, our results also revealed novel gene subsets that included TNFalpha-regulated and hyperthermia-unaffected genes, as well as genes (co)repressed, (co)stimulated, or antagonized by both types of stimuli. On Illumina platform we sequenced DNA immunoprecipitated from U-2 OS cells using anti-HSF1 antibody. Cells were either untreated (control) or heat shocked for 10 and 20 minutes. Two PCR-verified ChIP replicates were collected per each sample.

2015-08-01 | E-GEOD-60984 | biostudies-arrayexpress

Subsets of NFkappaB-dependent genes are differentially regulated after combined treatment with hyperthermia and cytokine

Project description:Heat shock transcription factor 1 (HSF1) is responsible for triggering stress-induced activation of the HSP genes. HSF1 is also involved in the regulation of many other genes associated with multiple cellular processes including cell signaling, development, fertility, cell death and metabolism, e.g. NFkappaB transcription factor. Here we aimed to establish a global picture for the association between hyperthermia-modulated expression of NFkappaB-dependent genes and HSF1 binding in regulatory regions of target genes. The global pattern of HSF1 binding was analyzed after 10 and 20 minutes of hyperthermia using the ChIP-Seq approach. The analysis revealed about 25,000 HSF1 binding sites in chromatin of control untreated U-2 OS cells, which nearly doubled in cells subjected to hyperthermia. The presence of hyperthermia-induced HSF1 binding was established in regulatory regions of hyperthermia-affected genes and in TNF-affected genes. In most cases hyperthermia pre-conditioning inhibited cytokine-mediated activation of NF-κB-dependent genes. However, our results also revealed novel gene subsets that included TNFalpha-regulated and hyperthermia-unaffected genes, as well as genes (co)repressed, (co)stimulated, or antagonized by both types of stimuli.

2015-08-01 | GSE60984 | GEO

Identification of genes regulated by HSF1 in control and heat-shocked cells

Project description:To examine the regulation of HSF1-mediated gene expression in control and heat shock conditions, we performed DNA microarray analysis. mRNA levels in control and heat-shocked MEF cells, which were infected with adenovirus expressing scramble RNA or HSF1 short hairpin RNA, were analyzed by DNA microarray analysis using GeneChip Mouse Gene 1.0 ST Array (Affymetrix).

2014-11-01 | E-GEOD-54060 | biostudies-arrayexpress

Identification of genes regulated by HSF1 in control and heat-shocked cells

Project description:To examine the regulation of HSF1-mediated gene expression in control and heat shock conditions, we performed DNA microarray analysis.

2014-11-01 | GSE54060 | GEO

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