The mammalian germline corrects deleterious effects of endocrine disruptors
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ABSTRACT:
PROVIDER: PRJNA255525 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-02-18 | E-GEOD-59543 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2015-02-18 | GSE59543 | GEO
Project description:We treated gestating female mice with vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays we detected changes in transcription and DNA methylation, respectively, in fetal prospermatogonia. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the subsequent generation. Pregnant mice were administered endocrine distruptors (VZ at 100 mg/kg/day, DEHP at 750 mg/kg/day, and BPA at 0.2 mg/kg/day) startin g at 12.5 days post coitum (dpc) and tissue samples were collected at 17.5 dpc.
2015-02-18 | E-GEOD-58642 | biostudies-arrayexpress
Project description:We treated gestating female mice with vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays we detected changes in transcription and DNA methylation, respectively, in fetal prospermatogonia. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the subsequent generation.
2015-02-18 | GSE58642 | GEO
Project description:Environmental reproductive health focuses on the effect of exposure to contaminants considered as endocrine disruptors. Developmental testis is considered as target of these compounds affecting testicular functions in adults and suspected implications in tumor etiology. Comparative analysis of gene expression in mouse testis exposed to five disruptors, three different dosages and three accumulative developmental stages shown defined signature profiles of gene deregulation for MEHP (monoethyl phthalate) and zearalenone (a phytoestrogen) and different to 17β-estradiol exposure. The effects are even detected in postpuberal male offspring from premating exposed mothers. Oxidative stress response, protein ubiquitination and oxidative phosphorylation are the most representative pathways affected.
2010-06-01 | GSE14774 | GEO
Project description:Genome wide anaylsis of rats exposed to endocrine disruptors.
| PRJNA540251 | ENA
Project description:According to recent reports, exposure to environmental endocrine disrupting chemicals (EDs) during pregnancy may harm multiple subsequent generations. We hypothesized that EDs must directly alter DNA methylation and/or transcription in the exposed fetal germ cells to affect the grandchild. In addition, the aberrant pattern must be retained in the germ cells of the grandchild -- withstanding global epigenome remodeling -- to affect the great-grandchild. To test this hypothesis, we extensively searched for immediate and persistent epigenetic effects in purified germ cells of the exposed fetus and those of the next generation. We treated gestating female mice with previously validated doses of vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays, we detected changes in transcription and DNA methylation in the exposed prospermatogonia but these did not persist into the prospermatogonia of the next generation. There was no evidence for transgenerational inheritance of these epigenetic aberrations. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the next generation. Pregnant mice were gavaged daily with endocrine distruptors (VZ at 100 mg/kg/day, DEHP at 750 mg/kg/day, BPA at 0.2 mg/kg/day or control oil) starting at 12.5 days post coitum (dpc) and the G1R germ cells were purified from the exposed fetuses at 17.5 dpc. The G2R germ cells were purified from fetuses that were sired by males that had been treated in utero in a G0 mother. G1R spermatozoa were collected from adult males that had been treated in utero at the fetal stages. G2R spermatozoa were collected from adult males who were sired by in-uteo-treated males.
2015-02-18 | E-GEOD-59539 | biostudies-arrayexpress
Project description:According to recent reports, exposure to environmental endocrine disrupting chemicals (EDs) during pregnancy may harm multiple subsequent generations. We hypothesized that EDs must directly alter DNA methylation and/or transcription in the exposed fetal germ cells to affect the grandchild. In addition, the aberrant pattern must be retained in the germ cells of the grandchild -- withstanding global epigenome remodeling -- to affect the great-grandchild. To test this hypothesis, we extensively searched for immediate and persistent epigenetic effects in purified germ cells of the exposed fetus and those of the next generation. We treated gestating female mice with previously validated doses of vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays, we detected changes in transcription and DNA methylation in the exposed prospermatogonia but these did not persist into the prospermatogonia of the next generation. There was no evidence for transgenerational inheritance of these epigenetic aberrations. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the next generation. Pregnant mice were gavaged daily with endocrine distruptors (VZ at 100 mg/kg/day, DEHP at 750 mg/kg/day, BPA at 0.2 mg/kg/day or control oil) starting at 12.5 days post coitum (dpc) and the G1R germ cells were purified from the exposed fetuses at 17.5 dpc. The G2R germ cells were purified from fetuses that were sired by males that had been treated in utero in a G0 mother. G1R spermatozoa were collected from adult males that had been treated in utero at the fetal stages. G2R spermatozoa were collected from adult males who were sired by in-uteo-treated males.
2015-02-18 | E-GEOD-59542 | biostudies-arrayexpress
Project description:Exposure to environmental endocrine-disrupting chemicals during pregnancy reportedly causes transgenerationally inherited reproductive defects. We hypothesized that to affect the grandchild, endocrine-disrupting chemicals must alter the epigenome of the germ cells of the in utero-exposed G1 male fetus. Additionally, to affect the great-grandchild, the aberration must persist in the germ cells of the unexposed G2 grandchild.Here, we treat gestating female mice with vinclozolin, bisphenol A, or di-(2-ethylhexyl)phthalate during the time when global de novo DNA methylation and imprint establishment occurs in the germ cells of the G1 male fetus. We map genome-wide features in purified G1 and G2 prospermatogonia, in order to detect immediate and persistent epigenetic aberrations, respectively. We detect changes in transcription and methylation in the G1 germline immediately after endocrine-disrupting chemicals exposure, but changes do not persist into the G2 germline. Additional analysis of genomic imprints shows no persistent aberrations in DNA methylation at the differentially methylated regions of imprinted genes between the G1 and G2 prospermatogonia, or in the allele-specific transcription of imprinted genes between the G2 and G3 soma.Our results suggest that endocrine-disrupting chemicals exert direct epigenetic effects in exposed fetal germ cells, which are corrected by reprogramming events in the next generation. Avoiding transgenerational inheritance of environmentally-caused epigenetic aberrations may have played an evolutionary role in the development of dual waves of global epigenome reprogramming in mammals.
| S-EPMC4376074 | biostudies-other
Project description:According to recent reports, exposure to environmental endocrine disrupting chemicals (EDs) during pregnancy may harm multiple subsequent generations. We hypothesized that EDs must directly alter DNA methylation and/or transcription in the exposed fetal germ cells to affect the grandchild. In addition, the aberrant pattern must be retained in the germ cells of the grandchild -- withstanding global epigenome remodeling -- to affect the great-grandchild. To test this hypothesis, we extensively searched for immediate and persistent epigenetic effects in purified germ cells of the exposed fetus and those of the next generation. We treated gestating female mice with previously validated doses of vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays, we detected changes in transcription and DNA methylation in the exposed prospermatogonia but these did not persist into the prospermatogonia of the next generation. There was no evidence for transgenerational inheritance of these epigenetic aberrations. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the next generation.
2015-02-18 | GSE59542 | GEO