Effects of the sex chromosome complement, XX, XO or XY, on the transcriptome and development of mouse oocytes during follicular growth.
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PROVIDER: PRJNA763388 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: To understand how sex chromosome complement, XX, XO and XY, influences the transcriptome in the oocytes of grwoth phase. Methods: Oocytes of 50 and 60 µm in diameter were isolated from mouse ovaries at 18 dpp and subject to RNA-sequencing. Results: (1) Many X-linked genes are subject to X chromosome dosage dependent expression. (2) Many genes are expressed from both short and long arms of the Y chromosome. (3) The transcriptome landscape in XY oocytes is closer to XX oocytes than XO oocytes. (4) About 10 genes are differentially expressed in XY oocytes compared to XX or XO oocytes. Conclusions: The differences in XY oocytes became exacerbated to differ from XX or XO oocytes near the end of growth phase.
2021-12-01 | GSE184153 | GEO
Project description: Not available
| S-EPMC8721172 | biostudies-literature
Project description:RNA-seq of in vitro produced mouse oocytes derived from XX-, XO- and XY-ESCs
| PRJNA496602 | ENA
Project description:Gobal expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice with the aim of identifying which genes are expressed from both X chromosomes as well as those genes deregulated in X chromosome monosomy. Keywords: Expression profiling by array For each tissue, the RNA samples of seven 40,XX, eight 39,XpO and eight 39,XmO mice were pooled by genotype into 9 groups, representing 3 biological replicates per genotype, as follows: 39,XpO-1 and 39,XpO-2 (3 pooled individuals each), 39,XpO-3 (2 pooled individuals); 39,XmO-1 and 39,XmO-2 (3 pooled individuals each), 39,XmO-3 (2 pooled individuals); 40,XX-1 and 40,XX-2 (3 pooled individuals each) 40,XX-3 (2 pooled individuals)
2010-04-07 | E-GEOD-13520 | biostudies-arrayexpress
Project description:Gobal expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice with the aim of identifying which genes are expressed from both X chromosomes as well as those genes deregulated in X chromosome monosomy. Keywords: Expression profiling by array
2010-03-12 | GSE13520 | GEO
Project description:The oocytes of B6.Y(TIR) sex-reversed female mouse mature in culture but fail to develop after fertilization because of their cytoplasmic defects. To identify the defective components, we compared the gene expression profiles between the fully-grown oocytes of B6.Y(TIR) (XY) females and those of their XX littermates by cDNA microarray. 173 genes were found to be higher and 485 genes were lower in XY oocytes than in XX oocytes by at least 2-fold. We compared the transcript levels of selected genes by RT-PCR in XY and XX oocytes, as well as in XO oocytes missing paternal X-chromosomes. All genes tested showed comparable transcript levels between XX and XO oocytes, indicating that mRNA accumulation is well adjusted in XO oocytes. By contrast, in addition to Y-encoded genes, many genes showed significantly different transcript levels in XY oocytes. We speculate that the presence of the Y-chromosome, rather than the absence of the second X-chromosome, caused dramatic changes in the gene expression profile in the XY fully-grown oocyte.
2013-04-02 | GSE45668 | GEO
Project description:The oocytes of B6.Y(TIR) sex-reversed female mouse mature in culture but fail to develop after fertilization because of their cytoplasmic defects. To identify the defective components, we compared the gene expression profiles between the fully-grown oocytes of B6.Y(TIR) (XY) females and those of their XX littermates by cDNA microarray. 173 genes were found to be higher and 485 genes were lower in XY oocytes than in XX oocytes by at least 2-fold. We compared the transcript levels of selected genes by RT-PCR in XY and XX oocytes, as well as in XO oocytes missing paternal X-chromosomes. All genes tested showed comparable transcript levels between XX and XO oocytes, indicating that mRNA accumulation is well adjusted in XO oocytes. By contrast, in addition to Y-encoded genes, many genes showed significantly different transcript levels in XY oocytes. We speculate that the presence of the Y-chromosome, rather than the absence of the second X-chromosome, caused dramatic changes in the gene expression profile in the XY fully-grown oocyte. We compared the gene expression profiles between the fully-grown oocytes of B6.Y(TIR) (XY) females and those of their XX littermates by cDNA microarray Mouse GV oocytes of B6.Y(TIR) were collected for RNA extraction and hybridization to Affymetrix microarray. We sought to extract the differentially expressed genes in the XY oocytes.
2013-04-02 | E-GEOD-45668 | biostudies-arrayexpress
Project description:Gonadal sex determining (GSD) genes that initiate fetal ovarian and testicular development and differentiation are expressed in the cells of the urogenital ridge that differentiate as somatic support cells (SSCs), i.e., granulosa cells of the ovary and Sertoli cells of the testis. To identify potential new mammalian GSD genes, we analyzed the gene expression differences between XX and XY SSCs cells isolated from the gonads of embryonic day (E) 13 mouse fetuses carrying an EGFP reporter transgene expressed specifically in SSCs. In addition, genome wide expression differences between XX and XY E13 whole gonads were examined. Newly identified differentially expressed transcripts are potential GSD genes involved in unexplained human sex reversal cases. Experiment Overall Design: Two seperate RNA samples were obtained from E13 XX and XY sorted EGFP+ cells, and two seperate RNA samples were obtained from E13 XX and XY pooled gonads. Approximately 20ng of total RNA from each sample was used to generate biotin-labelled cDNA. Approximately 2.5ug biotin labelled cDNA of each sample was used for each Mouse Genome 430v2.0 GeneChip array (Affymetrix). Significantly differentially expressed transcripts were identified using R/maanova. Statistical significance was determined at a false discovery rate value of equal to or less than 1%.
2007-11-30 | E-GEOD-4928 | 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:Abdominal aortic aneurysms (AAAs) are a prevalent and deadly human pathology with strong sexual dimorphism. Research demonstrates that sex hormones influence, but do not fully explain, male versus female AAA pathology. In addition to sex hormones, the X and Y sex chromosomes, and their unique complements of genes, may contribute to sexually dimorphic AAA pathology. Here, for the first time, we defined the effect of female (XX) versus male (XY) chromosome complement on AAA formation and rupture in phenotypically female mice using an established murine model. Abdominal aortas from female mice bearing the XY chromosome selectively expressed Y chromosome genes, while genes known to escape X-inactivation were higher in XX females. The majority of gene differences in XY females fell within inflammatory pathways. When XY females were infused with AngII, AAA incidences doubled and aneurysms ruptured. AAAs from XY females exhibited significant inflammation. Moreover, infusion of AngII to XY females augmented aortic activity of matrix metalloproteinases. Finally, testosterone exposure applied chronically, or as a single bolus at postnatal day 1, markedly worsened AAA outcomes in XY compared to XX females. These results demonstrate that an XY sex chromosome complement profoundly influences aortic gene expression profiles and promotes AAA severity.
2016-11-07 | GSE81580 | GEO