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The presence of the Y-chromosome, not the absence of the second X-chromosome, alters the mRNA levels stored in the fully grown XY mouse oocyte

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE45668 | GEO | 2013/04/02

SECONDARY ACCESSION(S): PRJNA195584

REPOSITORIES: GEO

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The presence of the Y-chromosome, not the absence of the second X-chromosome, alters the mRNA levels stored in the fully grown XY mouse oocyte

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

Effects of the sex chromosome complement, XX, XO or XY, on the transcriptome and development of mouse oocytes during follicular growth.

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

Transcriptional consequences of Zfy1 and Zfy2 expression in GV oocytes

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

Transcriptional consequences of Zfy1 and Zfy2 expression in GV oocytes

2013-11-27 | GSE52218 | GEO

Sex chromosome complement defines diffuse versus focal angiotensin II-induced aortic pathology

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

RNA-seq of in vitro produced mouse oocytes derived from XX-, XO- and XY-ESCs

Project description:RNA-seq of in vitro produced mouse oocytes derived from XX-, XO- and XY-ESCs

| PRJNA496602 | ENA

Potency of Testicular Somatic Environment to Support Spermatogenesis in XX/Sry Transgenic Male Mice

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

Effects of the sex chromosome complement, XX, XO or XY, on the transcriptome and development of mouse oocytes during follicular growth.

Project description:Effects of the sex chromosome complement, XX, XO or XY, on the transcriptome and development of mouse oocytes during follicular growth.

| PRJNA763388 | ENA

Generation of functional oocytes from male mice in vitro.

Project description:Sex chromosome disorder greatly compromises gametogenesis in both males and females. In oogenesis, the presence of a Y chromosome or the loss of an X chromosome disturbs the robust production of oocytes. In this study, we efficiently converted the XY chromosome set into two X chromosomes without an extra Y chromosome in mouse pluripotent stem cells (PSCs). In addition, this chromosomal alteration successfully eradicated trisomy 16 in PSCs, which is a model of Down syndrome. The artificially produced euploid XX PSCs differentiated into mature oocytes in culture as efficiently as native XX PSCs. Importantly, by this means, induced pluripotent stem cells (iPSCs) from the tail of a sexually mature male differentiated into fully potent oocytes, which gave rise to offspring after fertilization. This study provides insights that could lead to a cure for infertility caused by sex chromosome or autosomal disorders, and paves a way forward to bipaternal reproduction.

2022-12-27 | GSE184771 | GEO

XY female mice develop severe abdominal aortic aneurysms

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

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