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Smarca4 ChIP-seq in XX and XY mESCs

ABSTRACT: Smarca4 ChIP-seq in XX and XY mESCs

PROVIDER: PRJNA767662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16131113.fastq.gz	Fastqsanger.gz
	SRR16131114.fastq.gz	Fastqsanger.gz
	SRR16131115.fastq.gz	Fastqsanger.gz
	SRR16131116.fastq.gz	Fastqsanger.gz
	SRR16131117.fastq.gz	Fastqsanger.gz

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Smarca4 ChIP-seq in XX and XY mESCs

Project description:This experiment is designed to test if Smarca4 acts directly on the establishing inactive X chromosome

2022-02-02 | GSE185108 | GEO

RNA seq comparative analysis of XX, XY, and XXTet3-/- mutant mouse embryonic stem cells versus XX, XY, and XXTet3-/- mutant epiblast-like cells

Project description:In XXTet3-/- mESCs DNA methylation levels are higher than XX wildtype levels. We sought to determine if changes in cytosine modifications observed in XXTet3-/- mESCs impacted gene expression, we performed RNA-seq. 104 genes were up regulated in the mutant XX mESCs relative to wild type controls, and 86 were down regulated To ask whether the XX-specific nuclear enrichment of TET3 is necessary for a developmental transition, we differentiated WT XX and XXTet3-/- mESCs into epiblast-like cells (EpiLCs). Comparison of WT XX and XXTet3-/- EpiLC RNA-seq showed that 404 genes exhibited increased expression and 499 exhibited decreased expression in mutant cells. GO term analysis showed gene expression changes affecting several LIF and BMP signaling pathways. However, despite these changes in signaling pathway driven expression, the expression of mESC markers went down and mEpiLC markers went up comparably upon differentiation WT XX and XXTet3-/- mESCs, suggesting that many key transcriptional changes that characterize this transition can occur without TET3.

2022-09-01 | GSE171847 | GEO

Transcription profiling of XX and XY sorted mouse somatic support cells and XX and XY mouse whole gonads to identify potential new mammalian gonadal sex determining genes.

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

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

RNA seq comparative analysis of XX, XY, and XXTet3-/- mutant mouse embryonic stem cells versus XX, XY, and XXTet3-/- mutant epiblast-like cells

Project description:RNA seq comparative analysis of XX, XY, and XXTet3-/- mutant mouse embryonic stem cells versus XX, XY, and XXTet3-/- mutant epiblast-like cells

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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.

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SMARCA4 Rescue Profiling [ChIP]

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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

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Comparison of gene expression by RNA-seq in canine gonads from embryos at risk of XX Disorder of Sex Development (XX), male (XY) littermate controls, and age-matched female (XX) and male (XY) controls.

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.

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PolyA-tail enriched RNA-seq in differentiating TX1072 XX mESCs

Project description:PolyA-tail enriched RNA-seq in differentiating TX1072 XX mESCs

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