Transcriptome analysis of medaka germ cells and gonadal somatic cells during the gonadal sex differentiation.
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ABSTRACT:
ORGANISM(S): Oryzias latipes
PROVIDER: GSE59521 | GEO | 2014/08/31
SECONDARY ACCESSION(S): PRJNA255499
REPOSITORIES: GEO
Similar Datasets
Project description:Microarray analysis was performed using germ cells and gonadal somatic cells isolated by Fluorescence Activated Cell Sorter (FACS) from XX and XY embryos at st.33 and st.35. Medaka germ cells (olvas-EGFP) and somatic cells (sox9b-DsRed) were isolated by FACS. The microarray experiments were done using three independent biological replicates.
2014-08-31 | E-GEOD-59521 | biostudies-arrayexpress
Project description:Mammalian gonadal sex determination is dependent on proper expression of sex determining genes in fetal gonadal somatic support cells (i.e., pre-granulosa and pre-Sertoli cells in XX and XY gonads, resp.). We used a unique transgenic mouse strain combined with microarray profiling to identify all the differentially expressed transcripts in XX and XY isolated somatic support cells during critical stages of gonadal development and differentiation.
2009-11-09 | GSE18211 | GEO
Project description:Mammalian gonadal sex determination is dependent on proper expression of sex determining genes in fetal gonadal somatic support cells (i.e., pre-granulosa and pre-Sertoli cells in XX and XY gonads, resp.). We used a unique transgenic mouse strain combined with microarray profiling to identify all the differentially expressed transcripts in XX and XY isolated somatic support cells during critical stages of gonadal development and differentiation. Experiment Overall Design: XX and XY somatic support cells (SSC) were isolated by flow cytometry from embryonic day (E) 11.5 and E12.5 mouse gonads. Total RNA was isolated from pools of isolated cells; 3 pools per sex and each timepoint.
2009-11-13 | E-GEOD-18211 | 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. Keywords: microarray, mouse fetal gonadal somatic support cells, sex determination
2006-05-27 | GSE4928 | GEO
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:Sex differences in the brain as they relate to health and disease are often overlooked in experimental models. Many neurological disorders, like Alzheimer’s disease (AD), multiple sclerosis (MS), and autism, differ in prevalence between males and females. Sex differences originate either from differential gene expression on sex chromosomes or from hormonal differences, either directly or indirectly. To disentangle the relative contributions of genetic sex (XX v. XY) and gonadal sex (ovaries v. testes) to the regulation of hippocampal sex effects, we use the “sex-reversal” Four Core Genotype (FCG) mouse model which uncouples sex chromosome complement from gonadal sex. Transcriptomic and epigenomic analyses of hippocampal RNA and DNA from ∼12 month old FCG mice, reveals differential regulatory effects of sex chromosome content and gonadal sex on X- versus autosome-encoded gene expression and DNA modification patterns. Gene expression and DNA methylation patterns on the X chromosome were driven primarily by sex chromosome content, not gonadal sex. The majority of DNA methylation changes involved hypermethylation in the XX genotypes (as compared to XY) in the CpG context, with the largest differences in CpG islands, promoters, and CTCF binding sites. Autosomal gene expression and DNA modifications demonstrated regulation by sex chromosome complement and gonadal sex. These data demonstrate the importance of sex chromosomes themselves, independent of hormonal status, in regulating hippocampal sex effects. Future studies will need to further interrogate specific CNS cell types, identify the mechanisms by which sex chromosome regulate autosomes, and differentiate organizational from activational hormonal effects.
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Project description:Sex differences in the brain as they relate to health and disease are often overlooked in experimental models. Many neurological disorders, like Alzheimer’s disease (AD), multiple sclerosis (MS), and autism, differ in prevalence between males and females. Sex differences originate either from differential gene expression on sex chromosomes or from hormonal differences, either directly or indirectly. To disentangle the relative contributions of genetic sex (XX v. XY) and gonadal sex (ovaries v. testes) to the regulation of hippocampal sex effects, we use the “sex-reversal” Four Core Genotype (FCG) mouse model which uncouples sex chromosome complement from gonadal sex. Transcriptomic and epigenomic analyses of hippocampal RNA and DNA from ∼12 month old FCG mice, reveals differential regulatory effects of sex chromosome content and gonadal sex on X- versus autosome-encoded gene expression and DNA modification patterns. Gene expression and DNA methylation patterns on the X chromosome were driven primarily by sex chromosome content, not gonadal sex. The majority of DNA methylation changes involved hypermethylation in the XX genotypes (as compared to XY) in the CpG context, with the largest differences in CpG islands, promoters, and CTCF binding sites. Autosomal gene expression and DNA modifications demonstrated regulation by sex chromosome complement and gonadal sex. These data demonstrate the importance of sex chromosomes themselves, independent of hormonal status, in regulating hippocampal sex effects. Future studies will need to further interrogate specific CNS cell types, identify the mechanisms by which sex chromosome regulate autosomes, and differentiate organizational from activational hormonal effects.
2022-01-31 | GSE184013 | GEO
Project description:Expression profiles of XX and XY somatic gonadal compartment during sex determination. This experiment was updated in March 2011 to correct the incorrect age value for sample Female E10.5_6 (was 11 days should be 10.5).
2006-01-01 | E-MEXP-454 | 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 XX and XY- 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.
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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 autoantigen specific CD4+ T cells from XX and XY- 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 | GSE137793 | GEO