Expression data from 15-day-old mouse testes
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE128996 | GEO | 2019/03/29
REPOSITORIES: GEO
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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
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.
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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
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.
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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.
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