Sex-specific placental and fetal phenotypes in bovine at Midgestation (#108)
Fetal sex, along with maternal and paternal genome effects has pre- and postnatal phenotypic effects and a lifelong influence on an individual’s health. However, the magnitude of fetal sex effects on variation in placental and fetal traits at midgestation remains to be investigated. We used a bovine model and generated 73 fetuses with purebed and reciprocal cross Bos taurus and Bos indicus genetics and collected placenta, umbilical cord, total fetal fluids and fetal organs at day 153 of gestation. The largest placentome nearest to the fetus was weighed and processed for immunohistochemistry. Gross and histo-morphometric traits were analysed by general linear models with the fixed effects of sex and maternal and paternal genome. Our results show that parental genome contributes significantly (58-99%, P<0.05-0.001) to variation in placental and fetal phenotypes. Fetal sex contribution is highest to variation in maternal placenta weight (30%) and fetal brain (32%) and liver (30%) weights. Males have significantly heavier total placenta weight (P<0.05), maternal placenta (caruncle) weight (P<0.01), fetus weight (P<0.0001), fetal heart (P<0.05), liver (P<0.0001), and lung (P<0.001) weights. Males have better total placenta (P<0.01) and fetal placenta (fetal membranes plus cotyledons) efficiency than females and there is also a paternal genome by fetal sex interaction effect (P<0.05) on maternal placenta efficiency. Further, there are significant fetal sex-determined correlations between a) fetal placenta weight and maternal barrier thickness (P<0.05), b) umbilical cord weight and maternal placenta weight (P<0.05), c) umbilical cord length and fetal placenta weight (P<0.01), d) umbilical vein diameter with fetal heart weight (P<0.01), e) umbilical cord weight and fetal brain weight (P<0.0001). Our results show significant fetal sex-driven differences in placental and fetal traits. In humans, the male placenta is more efficient but may have lesser reserve capacity, because the male fetus invests maternal resources for its brain growth (Erikkson et al., 2010). Fetal sex-determined relationships between placental and fetal traits indicate the possibility that sex-specific genes trigger different sets of gene networks in the placenta (Sood et al., 2006; Osei-Kumah et al., 2011).