Canis lupus familiaris
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA357092 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5099670.fastq.gz | Fastqsanger.gz | |||
| SRR5099680.fastq.gz | Fastqsanger.gz | |||
| SRR5099690.fastq.gz | Fastqsanger.gz | |||
| SRR5099700.fastq.gz | Fastqsanger.gz | |||
| SRR5099710.fastq.gz | Fastqsanger.gz |
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Project description:In a rare subtype of XX Disorder of Sex Development (DSD), individuals are negative for SRY, the testis determining factor on the Y chromosome, yet develop testes or ovotestes, and both of these phenotypes occur in the same family. This is a naturally occurring disorder in humans (Homo sapiens) and dogs (C. familiaris), and phenotypes in the canine XX DSD model are strikingly similar to those in this type of human XX DSD. The purposes of this study were to identify 1) a variant associated with XX DSD in the canine model and 2) gene expression alterations in canine embryonic gonads that could be informative to causation. Using a genome wide association study (GWAS) and whole genome sequencing (WGS), we identified a variant on C. familiaris autosome 9 (CFA9) that is significantly associated with XX DSD in the canine model and in affected purebred dogs. This is the first marker and candidate causative variant identified for inherited canine XX DSD. It lies within the canine ortholog for the human disorder (OMIM 278850), which resides on 17q24, upstream of SOX9. Gene expression studies (RNA-seq and PRO-seq) in embryonic gonads at risk of XX DSD from the canine model identified significant RSPO1 downregulation in comparison to XX controls, without significant upregulation of SOX9 or other known testis pathway genes. A novel mechanism is proposed in which the canine XX DSD variant acts upstream of RSPO1 to induce epigenomic gonadal mosaicism.
2017-10-25 | GSE92283 | GEO
Project description:One of the earliest morphological changes during testicular differentiation is the establishment of an XY specific vasculature. The testis vascular system is derived from mesonephric endothelial cells that migrate into the gonad. In the XX gonad, mesonephric cell migration and testis vascular development is inhibited by WNT4 signaling. In Wnt4 mutant XX gonads, endothelial cells migrate from the mesonephros and form a male-like coelomic vessel. Consequently, the XX Wnt4 mutant mice presented an opportunity to focus a gene expression screen on the processes of mesonephric cell migration and testicular vascular development. We compared differences in gene expression between XY Wnt4+/+ and XX Wnt4+/+ gonads and between XX Wnt4-/- and XX Wnt4+/+ gonads to identify genes similarly upregulated in wildtype XY gonads and XX mutant gonads that might play important roles in testis-specific vascular development. Keywords: genetic sex and phenotypic comparisons
2005-11-24 | GSE3650 | GEO
Project description:Remarkable progress has been achieved in understanding the mechanisms controlling sex determination, yet the cause for many Disorders of Sexual Development remains unknown. Of particular interest is a rare XX DSD subtype in which individuals are negative for SRY, the testis determining factor on the Y chromosome, yet develop testes or ovotestes, and both phenotypes occur in the same family. This is a naturally occurring disorder in humans and dogs (Canis lupus familiaris), and phenotypes in the canine XX DSD model are strikingly similar to those in this type of human XX DSD. The purposes of this study were to identify 1) a variant associated with XX DSD in the canine model and 2) gene expression alterations in canine embryonic gonads that could be informative to causation. Using a genome wide association study (GWAS) and whole genome sequencing (WGS), we identified a variant on Canis familiaris autosome 9 (CFA9) that is significantly associated with XX DSD in the canine model and in affected purebred dogs. This is the first marker and candidate mutation identified for inherited canine XX DSD, and it lies within the canine ortholog for the human disorder (OMIM 278850). Inheritance of the variant indicates that XX DSD is a complex trait in which breed genetic background affects penetrance. Furthermore, the homozygous variant genotype is associated with embryonic lethality in at least one breed. Gene expression studies (RNA-seq and PRO-seq) in embryonic gonads at risk of XX DSD from the canine model identified significant RSPO1 downregulation without significant upregulation of SOX9 or other known testis pathway genes. A novel mechanism is proposed in which the canine XX DSD mutation acts upstream of RSPO1 to induce epigenomic gonadal mosaicism.
2017-10-02 | GSE92318 | 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:In mouse embryos, sex-specific differentiation of primordial germ cells (PGCs) begins with distinct cell cycle regulations: while PGCs in female (XX) gonads enter meiosis, PGCs in male (XY) gonads defer meiosis and arrest cell cycle1,2. The mitotic quiescence in XY gonads requires Nanos2, an evolutionarily conserved RNA-binding protein implicated in RNA degradation3-5; however, underlying mechanisms including the identity of its target mRNAs in vivo remain unknown. Here we show that Nanos2 negatively regulates Dazl (Deleted in azoospermia-like), a germline-specific gene encoding an RNA-binding protein that is implicated in translational control and meiotic initiation6,7. Comprehensive microarray analyses identified Dazl as one of the genes that were up-regulated in Nanos2-deficient XY gonads, but down-regulated in Nanos2-expressing XX gonads. Analysis of a BAC transgenic mouse line, in which the 3’UTR of Dazl can be removed by Flp-Frt recombination system, showed that repression of Dazl is likely achieved by the association of Nanos2 with Dazl’s 3’UTR. Elevated levels of Dazl expression in the transgenic XY PGCs resulted in abnormal progression of cell cycles including meiosis, reminiscent of the phenotype observed in Nanos2-/- XY gonads. This phenotype was suppressed by inhibiting retinoic acid (RA) signaling, suggesting that Nanos2 represses Dazl to prevent RA-induced cell cycle progression in XY PGCs. Furthermore, we show that a part of Nanos2-associated mRNAs, most of which are up-regulated in Nanos2-/- XY gonads, can also associate with Dazl, and that excess Dazl impedes localization of Nanos2 to processing-bodies where RNA degradation takes place, suggesting that repression of Dazl is required for Nanos2 to efficiently degrade its target mRNAs. These data provide the first link between the two RNA-binding proteins that play pivotal roles in sexual differentiation of murine PGCs.
2015-12-01 | GSE56794 | GEO
Project description:In mouse embryos, sex-specific differentiation of primordial germ cells (PGCs) begins with distinct cell cycle regulations: while PGCs in female (XX) gonads enter meiosis, PGCs in male (XY) gonads defer meiosis and arrest cell cycle1,2. The mitotic quiescence in XY gonads requires Nanos2, an evolutionarily conserved RNA-binding protein implicated in RNA degradation3-5; however, underlying mechanisms including the identity of its target mRNAs in vivo remain unknown. Here we show that Nanos2 negatively regulates Dazl (Deleted in azoospermia-like), a germline-specific gene encoding an RNA-binding protein that is implicated in translational control and meiotic initiation6,7. Comprehensive microarray analyses identified Dazl as one of the genes that were up-regulated in Nanos2-deficient XY gonads, but down-regulated in Nanos2-expressing XX gonads. Analysis of a BAC transgenic mouse line, in which the 3’UTR of Dazl can be removed by Flp-Frt recombination system, showed that repression of Dazl is likely achieved by the association of Nanos2 with Dazl’s 3’UTR. Elevated levels of Dazl expression in the transgenic XY PGCs resulted in abnormal progression of cell cycles including meiosis, reminiscent of the phenotype observed in Nanos2-/- XY gonads. This phenotype was suppressed by inhibiting retinoic acid (RA) signaling, suggesting that Nanos2 represses Dazl to prevent RA-induced cell cycle progression in XY PGCs. Furthermore, we show that a part of Nanos2-associated mRNAs, most of which are up-regulated in Nanos2-/- XY gonads, can also associate with Dazl, and that excess Dazl impedes localization of Nanos2 to processing-bodies where RNA degradation takes place, suggesting that repression of Dazl is required for Nanos2 to efficiently degrade its target mRNAs. These data provide the first link between the two RNA-binding proteins that play pivotal roles in sexual differentiation of murine PGCs.
2015-12-01 | GSE56793 | 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: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:Following sex determination, XY and XX gonads develop into a testis and an ovary, respectively. Depending on the sex of the gonad, resident germ cells will subsequently be committed to either spermatogenesis or oogenesis. In this study we took advantage of the Wv/Wv mouse genetic model, in which gonads are almost devoided of germ cells, to uncover gene expression underlying fetal germ cell development. Male and Female gonads were collected at 12, 14 and 16 days post coitum (dpc) from wild-type and Wv/Wv mouse embryos. Total RNAs were extracted and hybridized on Affymetrix microarrays. Expression signals from male and female gonads or from wild-type and mutant gonads were compared to identify sexually dimorphic genes as well as genes expressed in germ cell during fetal gonad development.
2010-12-20 | E-GEOD-23908 | biostudies-arrayexpress
Project description:Mice lacking the function of the PcG protein CBX2 (also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes. To clarify the molecular basis of the defects, RNA prepared from both wild type and KO gonads were subjected to microarray analyses. Mouse embryonic gonads of Cbx2 knockout (KO) were sectioned and recovered at E11.5 for RNA extraction and hybridization on Affymetrix microarrays. Four different genotypes of embryos at E11.5 (XY WT, XX WT, XY Cbx2 KO, and XX Cbx2 KO) were frozen in OCT compound without fixation. They were sectioned to 30 μm slices and stained with hematoxylin. The developing gonadal cells localized by GATA4 immunostaining and morphology were prepared using a Laser Microdissection System. The specimens prepared from two or three individuals were combined into one group, and three groups were prepared for each genotype.
2011-07-01 | E-GEOD-29485 | biostudies-arrayexpress