E-MTAB-6263
RNA-seq of estrogen (E2) induced changes of mRNA expression in male and female blastocysts.
Environmental estrogens may affect epigenetic programming as early as the period of preimplantation development. Therefore, we analyzed the effects of continuous gestational estradiol-17ß (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.
Environmental estrogens may affect epigenetic programming as early as the period of preimplantation development. Therefore, we analyzed the effects of continuous gestational estradiol-17ß (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.