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Constitutive expression of activated NOTCH1 in fetal Sertoli cells dysregulates factors required for proper gonocyte maintenance and survival.

ABSTRACT: Genome-wide analysis of whole embryonic day 14.5 mouse testes constitutively expressing the activated intracellular domain of NOTCH1 in Sertoli cells. The goal of the study was to identify Sertoli cell expressed genes regulated by Notch signaling, which are critical to gonocyte maintenance and survival. The mouse model was generated by intercrossing anti-Müllerian hormone (Amh)-cre transgenic mice and RosaNICD transgenic mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE37073 | GEO | 2013/02/08

SECONDARY ACCESSION(S): PRJNA158091

REPOSITORIES: GEO

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Constitutive expression of activated NOTCH1 in fetal Sertoli cells dysregulates factors required for proper gonocyte maintenance and survival.

Project description:Genome-wide analysis of whole embryonic day 14.5 mouse testes constitutively expressing the activated intracellular domain of NOTCH1 in Sertoli cells. The goal of the study was to identify Sertoli cell expressed genes regulated by Notch signaling, which are critical to gonocyte maintenance and survival. The mouse model was generated by intercrossing anti-Müllerian hormone (Amh)-cre transgenic mice and RosaNICD transgenic mice. Testes were dissected free from mesonephroi and testis pairs from a single fetus were pooled to generate a single sample. Littermates not expressing Amh-cre were used as controls. Testes from one control and one overexpressor fetus per dam from three separate dams were used for analysis.

2013-02-08 | E-GEOD-37073 | biostudies-arrayexpress

Microarrays analysis of RNA isolated from 7days-Sertoli cell culture of 14 day-old AMH-Cre/WT and WT/WT C57BL/6J mouse testes

Project description:In order to understand whether sole Cre recombinase expression has an effect on stress signalling pathways and the peroxisomal or other subcellular compartments, we have analyzed total RNA isolated from Sertoli cell cultures of anti-Müllerian-hormone (AMH)-Cre/wild-type and wild-type/wild-type C57BL/6J mouse testes using microarrays. The Sertoli cells were isolated from individual 14 day-old mice and were cultivated for 7 days. Total RNA was isolated from the Sertoli cell culture (for AMH-Cre/WT 5 mice and WT/WT 3 mice) and the same genotypes were pooled together. For the microarray analysis two technical replicates for each genotype were generated.

2012-01-01 | E-GEOD-28307 | biostudies-arrayexpress

Microarrays analysis of RNA isolated from 7days-Sertoli cell culture of 14 day-old AMH-Cre/WT and WT/WT C57BL/6J mouse testes

2012-01-01 | GSE28307 | GEO

Effects of deletion of Arhgef15 gene in mouse sertoli cells on spermatogenesis

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.

2022-06-16 | GSE206018 | GEO

Gene expression in 10 d Wild-type and Amh-cre Hdac3 KO Sertoli cells

Project description:This study aims to explore the transcriptional changes in Sertoli cells depleted with HDAC3. Sertoli cells were isolated from wild-type and Amh-cre Hdac3 KO mice at postnatal day 10.

2024-12-27 | GSE228746 | GEO

RiboTag analysis of actively translated mRNAs in Sertoli and Leydig cells in vivo

Project description:Analysis of Sertoli and Leydig cell “translatome” utilizing an in vivo ribosome tagging strategy (RiboTag) that allows a detailed and physiologically relevant characterization of the polysome-associated mRNAs in vivo. Although progress has been made in the identification of specific transcripts that are translated in Sertoli and Leydig cells and their response to hormones, efforts to expand these studies have been restricted by technical hurdles. Our analysis identified all previously characterized Leydig and Sertoli cell-specific markers and identified in a comprehensive manner novel markers of Leydig and Sertoli cells; the translational response of these two cell types to gonadotropins or testosterone was also investigated. Leydig cell-specific (Cyp17iCre: RiboTag) and Sertoli cell-specific (AMH-Cre: RiboTag) RiboTag mice were obtained by crossing RiboTag homozygous mice with Cyp17iCre or AMH-Cre mice. For in vivo LH treatment experiments, mice were injected with the GnRH antagonist acyline for 4 days before a single injection of purified human LH. After treatment, testes were homogenized and polysomes were immunoprecipitated by utilizing an anti-HA antibody. RNA was extracted, labelled, and hybridized to Mouse Gene ST 1.0 arrays.

2013-04-06 | E-GEOD-45799 | biostudies-arrayexpress

Osterix functions downstream of anti-Müllerian hormone signaling to regulate Müllerian duct regression

Project description:The goal of this study was to identify potential AMH-induced genes and regulatory networks controlling regression by RNA-Seq transcriptome analysis of differences in Müllerian Duct mesenchyme between males (AMH signaling on) and females (AMH signaling off) in purified fetal Müllerian Duct mesenchymal cells. This analysis found 82 genes up-regulated in males during MD regression and identified Osterix (Osx)/Sp7, a key transcriptional regulator of osteoblast differentiation and bone formation, as a novel downstream effector of AMH signaling during MD regression.

2018-07-16 | GSE116157 | GEO

Seminiferous tubule degeneration and infertility in mice with sustained activation of WNT/CTNNB1 signaling in sertoli cells

Project description:To elucidate the role(s) of WNT/CTNNB1 signaling in the testis, transgenic Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were generated to obtain sustained activation of the WNT/CTNNB1 pathway in Sertoli cells. Male Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ mice were sterile because of testicular atrophy starting at 5 wk of age, associated with degeneration of seminiferous tubules and the progressive loss of germ cells. Sustained WNT/CTNNB1 pathway activation was obtained in Ctnnb1 tm1Mmt/+;Amhr2 tm3(cre)Bhr/+ Sertoli cells. Sertoli cells often exhibited morphological characteristics suggestive of incomplete differentiation that appeared in a manner coincident with germ cell loss, accompanied by an increase in the expression of the immature Sertoli cell marker AMH. Microarray analyses performed on cultured Sertoli cells showed that CTNNB1 induces the expression of genes associated with the female sex determination pathway as well as cell-cycle associated genes . Together, these data suggest that the WNT/CTNNB1 pathway regulates Sertoli cell functions critical to their capacity to support spermatogenesis and to proliferate in the postnatal testis.

2011-04-05 | GSE28402 | GEO

Riding the spermatogenic wave: Profiling gene expression within neonatal germ and Sertoli cells during a synchronized initial wave of spermatogenesis

Project description:WIN 18,446/RA treatment of neonatal mice was used to synchronize the initial wave of spermatogenesis and identify novel messages expressed within either germ or Sertoli cells as spermatogonia enter meiosis. germ cell-specific (Stra8-cre: RiboTag; or Ngn3-cre:RiboTag) and Sertoli cell-specific (Amh-Cre: RiboTag)

2014-05-01 | E-GEOD-54408 | biostudies-arrayexpress

Single cell RNA sequencing of embryonic day 14.5 testes isolated from wild-type and mutant mice lacking Nr5a1 in Sertoli cells from embryonic day E13.5

Project description:To investigate the role of the nuclear receptor NR5A1 in testis after sex determination, we have analyzed mice lacking NR5A1 in Sertoli cells (SC) from embryonic day (E) 13.5 onwards. Ablation of Nr5a1 impairs the expression of genes characteristic of the SC identity (e.g., Sox9, Amh), causes SC death from E14.5 through a Trp53-independent mechanism related to anoikis, and induces disorganization of the testis cords. Together, these effects cause germ cells to enter meiosis and die. Single-cell RNA-sequencing experiments revealed that NR5A1-deficient SC change their molecular identity: some acquire a “pre-granulosa-like” identity, while other revert to a “supporting progenitor-like” cell identity, most of them being “intersex” because they express both testicular and ovarian genes. Fetal Leydig cells (LC) do not display significant changes, indicating that SC are not required beyond E14.5 for their emergence or maintenance. In contrast, adult LC were absent from the postnatal testes. In addition, adult mutant males display persistence of Müllerian duct derivatives, decreased anogenital distance and reduced penis length, which can be explained by the loss of AMH and testosterone synthesis due to SC failure.

2023-12-03 | GSE219271 | GEO

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