RNA-seq of estrogen (E2) induced changes of mRNA expression in male and female blastocysts.
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ABSTRACT:
PROVIDER: PRJEB23699 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2208530.fastq.gz | Fastqsanger.gz | |||
| ERR2208540.fastq.gz | Fastqsanger.gz | |||
| ERR2208550.fastq.gz | Fastqsanger.gz | |||
| ERR2208521.fastq.gz | Fastqsanger.gz | |||
| ERR2208531.fastq.gz | Fastqsanger.gz |
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Project description:RNA-seq of estrogen (E2) induced changes of mRNA expression in male and female blastocysts.
| PRJEB23699 | ENA
Project description:Environmental estrogens may affect epigenetic programming as early as the period of preimplantation development. Therefore, we analyzed the effects of continuous gestational estradiol-17β (E2) exposure on male and female embryos. A low dose, close to the no-observed effect level (NOEL - 10 µg E2/kg body weight(bw)/d), a high dose (1000 µg E2/kg bw/d) and carrier only, as control group, was fed to sows from insemination until sampling at day 10 of pregnancy, respectively. 36 samples (n = 5-7 per treatment group and sex) were analyzed by high throughput sequencing.In the high dose group, RNA-sequencing of single embryos revealed 982 differentially expressed genes (DEG) in the female but none in the male blastocysts. Moreover, 62 and 3 DEG were found in female and male embryos of the NOEL dose group, respectively. Thus, maternal E2 treatment during early pregnancy affected gene expression of the embryos at day 10, potentially constituting the basis for long-term adverse effects.
2018-10-16 | E-MTAB-6263 | biostudies-arrayexpress
Project description:X-chromosome reactivation (XCR) in early development was studied using transcriptome data from bovine male and female blastocysts derived by in vitro fertilization (IVF) or somatic cell nuclear transfer (SCNT). X-chromosome genes (X-genes) were upregulated almost twofold higher in female IVF blastocysts compared to that found in males. Since the mean expression levels of autosomal genes were relatively constant in both males and females, the upregulation of X-genes in female IVFs demonstrated a transcriptional sexual dimorphism between the sexes. X-genes were similarly expressed in inner cell mass and trophectoderm cells of female blastocysts, indicating no imprinted inactivation of paternal X in trophectoderm. Whereas the distribution of female-to-male expression ratios for autosomal genes was well balanced in IVFs, the distribution of X-genes was biased towards females such that approximately 80% of X- genes showed an increased level of expression. These observations of XCR and of X and autosomal gene expressions in IVFs were found in SCNTs, although to a lesser extent than that found in IVFs. We found that sham SCNT blastocysts, which underwent the same nuclear transfer procedures but retained their embryonic genome, closely mimicked that found with IVFs, and therefore, demonstrated that embryo manipulation itself did not interrupt XCR. In addition, from a heatmap of X-gene expression, we found a distinctive pattern between the sexes in which female SCNTs differed from male SCNTs and donor cells, but resembled female IVFs. Our findings that female IVFs, and to a lesser extent female SCNTs, undergo XCR, demonstrate that clonal reprogramming of bovine X chromosomes is incomplete and varies not only among local chromosomal regions but also among individual blastocysts.
2017-03-01 | GSE95311 | GEO
Project description:Adult male goldfish, exposed to estrogen (E2) implant, 1 day exposure See the following for further details; Marlatt VL, Martyniuk, CJ, Zhang, D, Xiong, H, Xia, X, Trudeau, VL, Moon, T. Tissue-specific auto-regulation of estrogen receptor subtypes and transcript profiling of estrogen-responsive genes in the neuroendocrine brain of male goldfish (Carassius auratus) exposed to 17beta-estradiol. J. Mol. Endocrinol. (accepted). Keywords: Estrogen effect on male goldfish hypothalamus, microarray
2007-05-10 | GSE7025 | GEO
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
Project description:Male embryos are reported to develop faster than female in the preimplantation stage. Therefore, male and female embryos can be considered phenotypically different as early as the preimplantation stage. Employing our sexing system of enhanced green fluorescent protein (EGFP) tagging X chromosomes, we compared the global gene expression pattern of male and female embryos at the blastocyst stage using DNA microarray. Keywords= sex differentiation Keywords= preimplantation embryo Keywords= genomic imprinting Keywords: comparative hybridization
2006-02-03 | GSE2934 | GEO
Project description:Smart-Seq of female and male blastocysts from mothers bearing the OgtT931A mutation
| PRJEB67811 | ENA
Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17β-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans.
2015-12-31 | GSE75208 | GEO
Project description:To examine the effect of E2 treatment for the miRNA expression, at 15 week old, female wiled type mice were ovariectomized, and after one week, estradiol (E2) was delivered at a concentration of 0.050 mg/kg body weight/day. 24 hours after chemical treatment, uteruses from mice treated with or without E2 were dissected.
2009-07-22 | GSE13858 | GEO
Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17β-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans. Primary human nasal epithelial cells from females were exposed to E2 for 24h prior to infection, then infected with an H3N2 strain of influenza a virus for 2 hours. At 24 and 48h post infection, hNECs were collected in Trizol for RNA extraction and hybridization on Affymetrix Human Gene ST 2.0 microarrays.
2015-12-31 | E-GEOD-75208 | biostudies-arrayexpress