Retinoic Acid Is Sufficient for the in vitro Induction of Mouse Spermatocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE77051 | GEO | 2016/06/16
SECONDARY ACCESSION(S): PRJNA309333
REPOSITORIES: GEO
Similar Datasets
Project description:To identify RA-regulated genes in mSSCs, we treated mSSCs with vehicle, RA and RA plus CHX. To characterize the induced spermatogenic cells by transcriptome profiling, we cultured mSSCs on pup Sertolic cells supplemented with RA. Induced differentiating spermatogonia and induced spermatocytes were collected after a 3-day- and 6-day-induction, respectively. We carried out RNA-seq analysis of samples after different treatment and samples from different in vitro induction stages.Two biological replicates were included for each sample.
2016-06-16 | E-GEOD-77051 | 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.
2012-08-22 | E-GEOD-40248 | 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 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.
2012-08-22 | GSE40248 | 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 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:To reveal distinct transcriptomes associated with various spermatogenic cells, including spermatogonial stem cells and all of their subsequent progeny, single-cell transcriptomes from Adult human spermatogonia, StaPut-enriched spermatocytes and spermatids, or unselected steady-state spermatogenic cells were used for Drop-Seq analysis. We used the 10x Genomics Chromium (Drop-Seq) to perform single-cell RNA-seq
2018-11-06 | GSE109037 | GEO
Project description:The kinase protein WNK1 is highly expressed and phosphorylated in the testis, suggesting possible functions in regulating male fertility. Indeed, conditional pachytene-spermatocyte Wnk1 knock-out mice generated using the novel Wnt7a-Cre failed to produce functional sperm which resulted from the primary spermatogenic arrest during mid-pachynema. Global transcriptomic approaches identified ‘translation’ as one of the impacted events in Wnk1-depleted spermatocytes.
2023-08-27 | GSE234068 | GEO
Project description:To reveal distinct transcriptomes associated with various spermatogenic cells, including spermatogonial stem cells and all of their subsequent progeny, single-cell transcriptomes from Adult ID4-EGFP+ spermatogonia (sorted for brightest or dimmest), StaPut-enriched spermatocytes and spermatids, or unselected steady-state spermatogenic cells were used for 10x Genomics analysis. The GFP-bright and dim phenotypes exhibit distinct fates when assayed by transplantation, with ID4-EGFPbright cells highly enriched for SSCs, and ID4-EGFPdim cells enriched for progenitors. We used the 10x Genomics Chromium (Drop-Seq) to perform single-cell RNA-seq
2018-11-06 | GSE109033 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179579 | GEO
Project description:INO80 is the catalytic subunit of the multi-subunit INO80-chromatin remodeling complex that has been implicated in DNA replication, repair, and transcription regulation. Ino80-deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes, due to incomplete synapsis and aberrant DNA double-strand break repair (DSBR) that leads to apoptosis. We explored the mechanism by which INO80 mediates meiotic progression. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WTspermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Further, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment, and in turn showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Further, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.
2021-12-21 | GSE179577 | GEO