Mus musculus
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REPOSITORIES: ENA
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Project description:Sry is sufficient to induce testis formation and subsequent male development of internal and external genitalia in chromosomally female mice and humans. In XX sex-reversed males such as XX/Sry-transgenic (XX/Sry) mice, however, testicular germ cells always disappear soon after birth due to germ cell autonomous defects. Therefore, it remains unclear whether or not Sry alone is sufficient to induce a fully functional testicular soma capable of supporting complete spermatogenesis in the XX body. Here we demonstrated that the testicular somatic environment of XX/Sry males is defective in the later phases of spermatogenesis. Spermatogonial transplantation analyses using XX/Sry male mice revealed that donor XY spermatogonia are capable of proliferating, entering meiosis and differentiating into the round spermatid stage. XY donor-derived round spermatids, however, were frequently detached from the XX/Sry seminiferous epithelia and underwent cell death, thereby preventing further progress beyond the elongated spermatid stage. In contrast, immature XY seminiferous tubule segments transplanted under XX/Sry testis capsules clearly displayed proper differentiation into elongated spermatids in the transplanted XY donor tubules. Microarray analysis of seminiferous tubules isolated from XX/Sry testes confirmed missing expression of several Y-linked genes and alterations in the expression profile of genes associated with spermatogenesis. Therefore, our findings indicate dysfunction of the somatic tubule components, probably Sertoli cells, of XX/Sry testes, supporting our hypothesis that Sry alone is insufficient to induce a fully functional Sertoli cell in XX mice. Keywords: comparative genomic hybridization
2007-07-15 | GSE5319 | GEO
Project description:Sry is sufficient to induce testis formation and subsequent male development of internal and external genitalia in chromosomally female mice and humans. In XX sex-reversed males such as XX/Sry-transgenic (XX/Sry) mice, however, testicular germ cells always disappear soon after birth due to germ cell autonomous defects. Therefore, it remains unclear whether or not Sry alone is sufficient to induce a fully functional testicular soma capable of supporting complete spermatogenesis in the XX body. Here we demonstrated that the testicular somatic environment of XX/Sry males is defective in the later phases of spermatogenesis. Spermatogonial transplantation analyses using XX/Sry male mice revealed that donor XY spermatogonia are capable of proliferating, entering meiosis and differentiating into the round spermatid stage. XY donor-derived round spermatids, however, were frequently detached from the XX/Sry seminiferous epithelia and underwent cell death, thereby preventing further progress beyond the elongated spermatid stage. In contrast, immature XY seminiferous tubule segments transplanted under XX/Sry testis capsules clearly displayed proper differentiation into elongated spermatids in the transplanted XY donor tubules. Microarray analysis of seminiferous tubules isolated from XX/Sry testes confirmed missing expression of several Y-linked genes and alterations in the expression profile of genes associated with spermatogenesis. Therefore, our findings indicate dysfunction of the somatic tubule components, probably Sertoli cells, of XX/Sry testes, supporting our hypothesis that Sry alone is insufficient to induce a fully functional Sertoli cell in XX mice. Experiment Overall Design: Whole testes and seminiferous tubules of XX/Sry and W/Wv males were used for microarray expression analysis using the Affymetrix GeneChip system (Affymetrix, CA). In order to isolate the seminiferous tubules, the tunica was carefully removed from the testes which were then incubated in the medium with 5 mg/ml collagnease at 37oC for 40 min. The remaining seminiferous tubules were washed several times with PBS using a 70-ºm cell strainer to remove interstitial cells. After total RNA was extracted using a RNeasy Mini Kit (Qiagen, Germantown, MD), double-stranded cDNA and biotin-labeled cRNA were synthesized using One-Cycle cDNA Synthesis and IVT Labeling kits (Affymetrix, CA), respectively. Twenty micrograms of fragmented biotin-labeled cRNA was hybridized to the Affymetrix Mouse Expression Array MOE 430A for 16 hr at 45oC. The chips were washed, stained, and then scanned with the GeneArray Scanner (Hewlett Packard, CA) in accordance with the manufacturer's standard protocols. Finally, the microarray data were analyzed using Microarray Suite ver. 5.0 (Affymetrix). Differential expression was defined as a difference of 2-fold or more in both whole testis and seminiferous tubule samples between two recipient males. Mouse 430A Affymetrix Genome Array IDs were used to query the NetAffx data mining tool for gene annotations.
2008-06-13 | E-GEOD-5319 | biostudies-arrayexpress
Project description:Transcriptome analyses of fetal and adult Leydig cells
| PRJDB4234 | ENA
Project description:The purpose of this experiment was to determine the expression traits in Liver tissue from the Four Core Genotype treated group. Keywords: Sry transgene Four Core Genotype Mouse liver Tissue Liver tissue from the "Four Core Genotype" treated group consists of 20 female and male C57BL/6J mice fed a chow diet containing 4% fat (Ralston-Purina Co., St. Louis, MO) until 8 weeks of age and then were gonadectomized at 8 weeks of life. In mice of the "four core genotypes" (FCG), the Y chromosome is deleted for the testis-determining gene Sry, producing the Y- chromosome. The Sry transgene is inserted onto an autosome, so that testis determination is independent of the complement of sex chromosomes. XY-Sry gonadal males are bred with XX gonadal females, producing progeny with four different genotypes: two types of gonadal males (XX.Sry and XY-Sry) and two types of gonadal females (XX and XY-). At 12 weeks mice were sacrificed, after a 12-hour fast, Liver tissue were dissected and flash frozen in LN2 and stored at -80°C. All sample were compared to a common pool created from equal portions of RNA from each of the samples.
2010-06-24 | E-GEOD-13264 | biostudies-arrayexpress
Project description:Objective-Aortic pathologies exhibit sexual dimorphism, with aneurysms in the ascending, thoracic and abdominal aorta (AAA) exhibiting higher prevalence in males. Despite lower incidence of aortic vascular disease in women, aneurysms progress rapidly. Mechanisms for these sex differences are unclear. We defined the role of sex chromosome complement and testosterone in regional development and progression of angiotensin II (AngII)-induced vascular pathologies. Approach and Results-We used transgenic male mice expressing Sry on an autosome to create low density lipoprotein receptor (Ldlr) deficient male mice with an XY or XX sex chromosome complement. Subjects were then sham operated or orcheictomized. Transcriptional profiling on abdominal aortas from XY or XX males demonstrated1746 genes influenced by sex chromosomes, sex hormones, or an interaction. A second cohort of animals was then infused with AngII for 28 days. Diffuse aortic aneurysm pathology developed in XY AngII-infused males, while XX males developed discrete AAAs. Castration reduced all AngII-induced aortic pathologies in XY and XX males. Thoracic aortas from AngII-infused XY males, but not XX males exhibited adventitial thickening. We infused male XY and XX mice with saline or AngII and quantified mRNA abundance of key genes in thoracic versus abdominal aortas. Regional differences in mRNA abundance existed before AngII infusions, which were differentially influenced by AngII between genotypes. Prolonged AngII infusions resulted in AAA aortic wall thickening in XY males with diffuse aortic pathology, while XX males had dilated focal AAAs. Conclusions-An XY sex chromosome complement mediates diffuse aortic pathology, while an XX sex chromosome complement contributes to discrete AngII-induced AAAs.
2018-07-22 | GSE102143 | GEO
Project description:Sex-reversed ‘XYSry-’ female mice that lack Sry due to the 11 kb deletion Srydl1Rlb have very limited fertility, partly due to the effects of posessing only a single X chromosome. However, the fertility deficit is even worse in sex-reversed XY females than in XO females, implicating Y-linked genes in the further loss of fertility. Transgenic addition of Yp-linked genes to XO females and also to normal XX females implicated Zfy2 (but not the related Zfy1) as the cause of this effect. This study examines the transcriptional effects of Zfy2 and Zfy1 in GV oocytes from normal XX females. 18 samples representing 3 biological replicates from each of 6 genotypes. Genotypes are XX (normal control); XX,Zfy2-nf (control with non-functional Zfy2 transgene); XX,Zfy2 (with Zfy2 transgene); XX,Zfy2+Eif2s3y (contaminated sample, XX with Zfy2 transgene and also an Eif2s3y transgene in proportion of the cells), XX,Zfy1-lo (with single-copy Zfy1 transgene); XX-Zfy1-hi (with multi-copy Zfy1 transgene).
2013-11-27 | E-GEOD-52218 | biostudies-arrayexpress
Project description:To examine the transcriptome of early testicular somatic cells during gonadogenesis at 12.5dpc RNA sequencing (RNA-Seq) was performed on murine primary testicular cell lineages isolated from the Sf1-eGFP line by FACS. The three main somatic cell lineages of the testis were isolated: the Sertoli cells which direct male development; the fetal Leydig cells (FLCs) that produce steroid hormones and virilise the XY individual and a heterogenous population of interstitial cells, some of which give rise to the adult Leydig cells (ALCs). This dataset provides a platform for exploring the biology of FLCs and understanding the role of these cells in testicular development and masculinization of the embryo, and a basis for targeted studies designed to identify causes of idiopathic XY DSD. RNA-Seq of 3 enriched cell populations from 12.5dpc mouse gonad (Sertoli cells, Leydig cells and Interstitial cells isolated by FACS-sorting) on an Illumina HiSeq 1500, in triplicate.
2015-05-21 | E-GEOD-65498 | biostudies-arrayexpress
Project description:To determine the role of sex chromsomes in sex differences of autoimmune disease, we used high throughput RNA sequencing to analyze the transciptomes of CD4+ T cells stimuated with antiCD3/CD28 from XXSry and XY-Sry mice using the “four core genotypes” mouse model. We found higher expression of several X genes in the XY- genotype compared to XX, suggesting a difference in DNA methylation of these genes between Xp and Xm. In a hypothesis driven targeted approach, we investigated two immunomodulatory X genes, Tlr7 and FoxP3 and found that the promoter regions of both genes had more DNA methylation on the Xp than Xm, and that both genes had higher expression in autoantigen stimulated CD4+ T cells from XY- compared to XX mice. This study provides new insights regarding how sex chromsomes affect gene expression and cause sex differences in autoimmune disease.
2019-12-10 | GSE139034 | GEO