E-TABM-426
Ontology highlight
ABSTRACT:
PROVIDER: E-TABM-426 | ExpressionAtlas | 2014-08-16
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-TABM-426-analysis-methods.tsv | Tabular | |||
| E-TABM-426-atlasExperimentSummary.Rdata | Rdata | |||
| E-TABM-426-configuration.xml | Xml | |||
| E-TABM-426-percentile-ranks.tsv | Tabular | |||
| E-TABM-426.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 75 |
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Project description:We used two Sertoli-cell-specific Cre lines: Wt1-CreERT2 and Sox9-CreERT2, to induce Sox9 ablation on a Sox8 -/- background in the adult testis. Sox9/8 double KO testes undergo testis-to-ovary genetic reprogramming and Sertoli-to-granulosa cell transdifferentiation.
2016-06-08 | E-MTAB-4572 | biostudies-arrayexpress
Project description:ERM knockout mice were produced. Testis develop a Sertoli cell only syndrome, which appears complete by 10 weeks of age in male ERM knockout mice. Three sets of Affymetrix comparisons were made. #1 and #2, Wt or ERM knockout testis from 4 week old males, totaly RNA. This time preceeds any significant histologic difference between the wt or knockout. The results was the finding that only a very specific set or markers for spermatogonial STEM CELLs were found to be greatly reduced in the ERM knockout. #3 and #4. The sertoli cell line TM4 was transduced with a retroviral ERM. The wild type TM4 cell line was compared to this TM$-ERM cell line, with the finding that only a few genes were increased in the TM4-ERM line. #5, #6 and #7. Primary Sertoli cells were purified from 4 week old wild type or ERM knockout or from 10 week old ERM knockout mice and compared. Keywords: other
2005-04-01 | GSE2205 | GEO
Project description:ERM knockout mice were produced. Testis develop a Sertoli cell only; syndrome, which appears complete by 10 weeks of age in male ERM knockout mice. Three sets of Affymetrix comparisons were made. #1 and #2, Wt or ERM knockout testis from 4 week old males, totaly RNA. This time preceeds any significant histologic difference between the wt or; knockout. The results was the finding that only a very specific set or; markers for spermatogonial STEM CELLs were found to be greatly reduced in the ERM knockout. #3 and #4. The sertoli cell line TM4 was transduced with a retroviral; ERM. The wild type TM4 cell line was compared to this TM$-ERM cell line,; with the finding that only a few genes were increased in the TM4-ERM line. #5, #6 and #7. Primary Sertoli cells were purified from 4 week old wild; type or ERM knockout or from 10 week old ERM knockout mice and compared.
2008-06-11 | E-GEOD-2205 | biostudies-arrayexpress
Project description:Taf7l (a paralogue of Taf7) and Trf2 (a TBP-related protein) are components of the core promoter complex required for gene/tissue-specific transcription of protein-coding genes by RNA polymerase II. Previous studies reported that Taf7l knockout mice exhibit structurally abnormal sperm, reduced sperm count, weakened motility and compromised fertility. Here we find that continued backcrossing of Taf7l-/Y mice from N5 to N9 produced KO males that are essentially sterile. Genome-wide expression profiling by mRNA-seq analysis of wild type (WT) and Taf7l-/Y (KO) testes revealed that Taf7l ablation impairs the expression of many post-meiotic spermatogenic specific as well as metabolic genes. Importantly, histological analysis of testes revealed that Taf7l-/Y mice develop post-meiotic arrest at the first stage of spermiogenesis, phenotypically similar to Trf2-/- mice, but distinct from Taf4b-/- mice. Indeed, we find that Taf7l and Trf2 co-regulate post-meiotic genes, but none of Taf4b-regulated germ stem cell genes in testes. Genome-wide ChIP-seq studies indicate that TAF7L binds to promoters of activated post-meiotic genes in testis. Moreover, biochemical studies show that TAF7L associates with TRF2 both in vitro and in testis suggesting that TAF7L likely cooperates directly with TRF2 at promoters of a subset of post-meiotic genes to regulate spermiogenesis. Our findings thus provide a new mechanism for cell-type specific transcriptional control involving an interaction between a ‘non-prototypic’ core promoter recognition factor (Trf2) and an orphan TAF subunit (Taf7l) in mammalian testis-specific gene transcription. Genome-wide mapping of TAF7L and Pol II in testis tissue, and mRNA-seq expression profiling wild type and Taf7l knockout testis.
2013-09-29 | E-GEOD-50807 | biostudies-arrayexpress
Project description:An excess in thyroid hormone during rodent neonatal life causes abnormal prolifration and maturation of testicular cells, leading to reduced testis size and impairments in steroidogenesis, Sertoli cell function, spermatogenesis and fertility. The high expression of type 3 deiodinase in the neonatal testis protects this tissue from premature exposure to thyroid hormones, since this gene (Dio3) function is to degrade thyroid hormones. DIO3-deficient mice (Dio3KO) exhibit a marked reduction in Sertoli cell proliferation and testis size, abnormalities in the reproductive axis and impaired fertility (Martinez et al. 2016, Endocrinology157:1276). To identify genes that are untimely regulated by thyroid hormone in the developing testes, we have performed RNAseq in testis total RNA from wild type and DIO3KO mouse neonates.
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Project description:Spermatogenesis is dependent primarily on testosterone action on the Sertoli cells. Although the identification of testosterone-regulated target genes in Sertoli cells has been approached using microarray analysis to compare gene expression in mice with androgen receptor (AR) elimination in the Sertoli cells (SCARKO) and wild type mice, the analysis has been complicated by alteration of germ cell composition of the testis when pubertal or adult mice were used and differences in Sertoli-cell gene expression from those in adult when prepubertal mice were used. Since the testicular cell components of adult jsd (Utp14bjsd ,juvenile spermatogonial depletion) mice and SCARKO-jsd mice are essentially identical, consisting of only type A spermatogonia and somatic cells, comparisons of gene expression profiles between jsd and SCARKO-jsd testes would identify AR regulated genes in adult Sertoli cells, with minimum effects of cell number changes. Microarray analysis identified 161 genes as downregulated and 202 genes as upregulated in the SCARKO-jsd mice compared to jsd mice. Some of the genes identified in the previous studies, including Rhox5, Drd4, and Fhod3, were also AR-regulated in the jsd testes but others, such as proteases and components of junctional complexes, were not androgen regulated in our model. Surprisingly, a set of germ-cell-specific genes preferentially expressed in differentiated spermatogonia and meiotic cells, including Meig1, Sycp3, and Ddx4, were all upregulated about 2-fold in SCARKO-jsd testes, demonstrating that, although there was no significant differentiation to spermatocytes in SCARKO-jsd mice, AR-regulated genes in Sertoli cells are involved in the regulation of spermatogonial differentiation. Further gene ontogeny analysis revealed possible sets of genes whose expression changes may be involved in the disruption of Sertoli cell organization in SCARKO-jsd testes. Comparisons of gene expression profiles between the testis of jsd mice (n=3) and SCARKO-jsd mice (n=3).
2010-09-06 | E-GEOD-20918 | biostudies-arrayexpress
Project description:Assess the transcriptomic effects of Sertoli-specific ablation of Dicer in mice
2009-01-06 | E-TABM-426 | biostudies-arrayexpress
Project description:Dmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. This study examines the result of conditional removal of Dmrt1 from Sertoli cells in P28 testis tissue. Testes from P28 Dmrt1 flox/flox mice were compared to testes from P28 Dmrt1 flox/flox mice with the Sertoli cell-specific Sf1 (Nr5a1; MGI:1346833) or Dhh (MGI:94891) promoters driving Cre expression.
2011-07-28 | E-GEOD-27261 | biostudies-arrayexpress
Project description:Sertoli cells, which are the only somatic cells in the seminiferous tubules, facilitate the maintenance of testicular immune privilege through the formation of the blood-testis barrier (BTB) and the expression of immunoregulatory factors. Rho guanosine exchange factor 15 (ARHGEF15) is a member of guanosine exchange factors, which are involved in cell migration, cell polarity, and cell cycle progression via activation of Rho GTPases. This study investigated the functions of ARHGEF15 in Sertoli cells during spermatogenesis using Sertoli cell–specific Arhgef15 knockout mice. The results showed that Arhgef15 deficiency in Sertoli cells affected the localization of Sertoli cell nuclei, disrupted BTB integrity, and led to premature shedding of germ cells. In Arhgef15flox/flox/Amh-Cre+ mice, the ultrastructure of the round spermatids was impaired, accompanied by acrosome degeneration, acrosomal vesicle shedding, and atrophic nuclei. Consequently, the percentage of abnormal sperm in the Arhgef15flox/flox/Amh-Cre+ epididymis was markedly elevated. RNA-sequencing analysis revealed that most of the differentially expressed genes in Sertoli cells of Arhgef15flox/flox/Amh-Cre+ mice were related to immunity. Further study revealed that the sera of Arhgef15flox/flox/Amh-Cre+ mice showed immunoreactivity against testicular lysate of wild-type mice, indicating the production of antibodies against testicular autoantigens in Arhgef15flox/flox/Amh-Cre+ mice. In conclusion, the specific deletion of Arhgef15 in Sertoli cells leads to sperm abnormality, probably by disrupting the testicular immune homeostasis, in mice.
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Project description:In mammals, male fate is under the control of the master transcriptional regulator, SOX9: in its presence, somatic precursor cells of the embryonic gonads differentiate into Sertoli cells, the main organizers of testicular differentiation. Therefore, analyzing target genes of this transcription factor allows understanding mechanisms of cellular commitment at the genomic level. With the use of ChIP-seq in murine and bovine wild-type testes combined with RNAseq from mouse testes lacking SOX9, we identified SOX9 target genes in the mammalian fetal gonad. SOX9 in murine and bovine fetal testes binds to a large set of genes conserved among mammals, including those with well-established roles in testis and ovary development. RNAseq analysis shows that testis and ovary display sex specific RNA splicing and that SOX9 mediates both target gene transcription and differential splicing. Regions bound by SOX9 are predominantly 5’ proximal or intra-genic, and display a specific genomic features that we call "Sertoli cell signatures" or SCS. The SCS is conserved among mammals and comprises multiple binding motifs for the Sertoli reprogramming factors SOX9, GATA4 and DMRT1; indeed, independent DMRT1 ChIP-seq confirms the enrichment of the SCS. Bioinformatic analysis of SCSs regions predicts novel regulatory mechanisms prompting functional validation. For example, we detected SCS in target genes of the nuclear factor TRIM28 and we show experimentally that SOX9 and TRIM28 proteins interact in fetal testis.
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