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Sex-related transcriptional differences in Day 7 bovine in vitro produced blastocysts

ABSTRACT: Sexual dimorphism in mammals is mostly attributable to sex-related hormonal differences in fetal and adult tissues; however, this may not be the sole determinant. Though genetically-identical for autosomal chromosomes, male and female preimplantation embryos could display sex-specific transcriptional regulation which can only be attributted to the differences in sexual chromosome dosage. We used microarrays to analyze sex-related transcriptional differences at the blastocyst stage.

ORGANISM(S): Bos taurus

PROVIDER: GSE17921 | GEO | 2010/02/24

SECONDARY ACCESSION(S): PRJNA119881

REPOSITORIES: GEO

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Project description:Sexual dimorphism in mammals is mostly attributable to sex-related hormonal differences in fetal and adult tissues; however, this may not be the sole determinant. Though genetically-identical for autosomal chromosomes, male and female preimplantation embryos could display sex-specific transcriptional regulation which can only be attributted to the differences in sexual chromosome dosage. We used microarrays to analyze sex-related transcriptional differences at the blastocyst stage. Day 7 bovine in vitro produced bovine blastocysts produced with sorted semen from 3 different bulls. Pooled RNA from 60 blastocysts of one sex and produced with one bull was used per chip. Three replicates of each sex per bull. In total, 18 Bovine GeneChip (Affymetrix) were used (3 replicates X 3 bulls X 2 sexes).

2010-03-09 | E-GEOD-17921 | biostudies-arrayexpress

Sexual dimorphism in early osteoclasts demonstrates enhanced inflammatory pathway activation in female cells

Project description:Sexual dimorphism of the skeleton is well documented. At maturity, the male skeleton is typically larger and has a higher bone density than the female skeleton. However, the underlying mechanisms for these differences are not completely understood. In this study, we examined sexual dimorphism in the formation of osteoclasts between cells from female and male mice. We found that the number of osteoclasts in bones was greater in females. Similarly, in vitro osteoclast differentiation was accelerated in female osteoclast precursor (OCP) cells. To further characterize sex differences between female and male osteoclasts, we performed gene expression profiling of cultured, highly purified, murine bone marrow OCPs that had been treated for 3 days with M-CSF and RANKL. We found that 125 genes were differentially regulated in a sex-dependent manner. In addition to genes that are contained on sex chromosomes, transcriptional sexual dimorphism was found to be mediated by genes involved in innate immune and inflammatory response pathways. Furthermore, the NFκB-NFATc1 axis was activated earlier in female early osteoclasts, which partially explains the differences in transcriptomic sexual-dimorphism in these cells. Collectively, these findings identify a sex-dependent intrinsic difference in early osteoclasts, which results from an altered response to osteoclastogenic stimulation. In humans these differences could contribute to the lower peak bone mass and increased risk of osteoporosis that females demonstrate relative to males.

2021-05-14 | GSE153299 | GEO

Role of sex chromosome complement in autosomal gene expression

Project description:It has generally been assumed that most differences between males and females are due to developmental and hormonal differences between the sexes. Here we investigate the contribution of sex chromosomal complement to such sexual dimorphisms. These genome-wide transcription profiling showed that the expression of hundreds of autosomal genes was sensitive to sex chromosome complement, rather than gender. The existence of such differences between males and females holds important implications for understanding sexual dimorphisms in physiology and disease hitherto attributed solely to gender or hormonal effects.

2010-10-02 | GSE21822 | GEO

Polymorphism in estrogen receptor binding site causes CD2-dependent sex bias in T cell autoimmune diseases

Project description:Complex autoimmune diseases are sexually dimorphic. An interplay between predisposing genetics and sex-related factors likely determines the sex discrepancy in the immune response, but conclusive evidence regarding the underlying molecular mechanisms is lacking. Using forward genetics, we positionally identified a polymorphic estrogen receptor binding site that regulates CD2 expression, leading to female-specific differences in mouse models of T cell-dependent autoimmunity. Female mice with reduced CD2 levels displayed a diminished T cell activation and autoimmune T cell response. Mechanistically, CD2 affected LAG-3 expression. Our findings help to explain the sexual dimorphism in human autoimmunity, as CD2 associated with rheumatoid arthritis and its regulation through 17-β-estradiol was conserved in human T cells. Hormonal regulation of CD2 has implications for CD2-targeted therapy. Indeed, anti-CD2 treatment more potently affected female mice. In conclusion, our results demonstrate the relevance of sex-genotype interactions and deliver strong evidence for CD2 as a sex-sensitive predisposing factor in autoimmunity.

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Sexual dimorphism in skin immunity is mediated by androgen-ILC2-dendritic cell axis [Bulk RNA-seq]

Project description:Males and females exhibit profound differences in immune responses and disease susceptibility. However, the factors responsible for sex differences in tissue immunity remain poorly understood. Here, we uncover a dominant role for type 2 innate lymphoid cells (ILC2) in shaping sexual immune dimorphism within the skin. Mechanistically, negative regulation of ILC2 by androgens leads to a reduction in dendritic cell (DC) accumulation and activation in males, and reduced tissue immunity. Collectively, this work uncovers an androgen-ILC2-DC axis in controlling sexual immune dimorphism. Moreover, this work proposes that tissue immune set-points are defined by the dual action of sex hormones and the microbiota, with sex hormones controlling the strength of local immunity and microbiota calibrating its tone.

2024-04-09 | GSE253293 | GEO

Sexual dimorphism in skin immunity is mediated by androgen-ILC2-dendritic cell axis [scRNA-seq]

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Role of sex chromosome complement in autosomal gene expression

2010-10-02 | E-GEOD-21822 | biostudies-arrayexpress

Comparison of gene expression in male and female blastocysts

Project description:It is basically understood that male and female development is initiated by gonad differentiation into either testis or ovary. However, male embryos are reported to develop faster than female during preimplantation, implying sex differences at this stage. To learn more about when sex differentiation begins, we compared the global gene expression pattern of male and female embryos at the blastocyst stage. First, Blastocyst samples were sexed, using a novel method for non-invasive sexing of preimplantation stage mouse embryos by tagging the X chromosome with an EGFP transgene, Next, gene expression patterns of the male and female were compared using DNA microarray.

2010-03-31 | GSE15611 | GEO

Changes in chromatin accessibility in mouse liver following a pulse of GH-activated liver STAT5 activity

Project description:This SuperSeries is composed of the SubSeries listed below. These files are part of a larger study where we establish that pulsatile chromatin opening stimulated by endogenous, physiological hormone pulses is a novel mechanism for establishing widespread sex differences in chromatin accessibility and transcription factor binding, which are closely linked to sex-biased gene expression and the sexual dimorphism of liver function.

2023-08-21 | GSE131853 | GEO

Spenito-dependent metabolic sexual dimorphism intrinsic to fat storage cells

Project description:Metabolism in males and females is distinct. Differences are usually linked to sexual reproduction, with circulating signals (e.g. hormones) playing major roles. By contrast, sex differences prior to sexual maturity and intrinsic to individual metabolic tissues are less understood. We analyzed Drosophila melanogaster larvae and find that males store more fat than females, the opposite of the sexual dimorphism in adults. We show that metabolic differences are intrinsic to the major fat storage tissue, including many differences in the expression of metabolic genes. Our previous work identified fat storage roles for Spenito (Nito), a conserved RNA-binding protein and regulator of sex determination. Nito knockdown specifically in the fat storage tissue abolished fat differences between males and females. We further show that Nito is required for sex-specific expression of the master regulator of sex determination, Sex-lethal (Sxl). “Feminization” of fat storage cells via tissue-specific overexpression of a Sxl target gene made larvae lean, reduced the fat differences between males and females, and induced female-like metabolic gene expression. Altogether, this study supports a model in which Nito autonomously controls sexual dimorphisms and differential expression of metabolic genes in fat cells in part through its regulation of the sex determination pathway.

2023-04-25 | GSE229991 | GEO