DOI: 10.1101/473967Nov 20, 2018Paper

Fetal and trophoblast PI3Kp110α have distinct roles in regulating resource supply to the growing fetus

BioRxiv : the Preprint Server for Biology
Jorge Lopez-TelloAmanda N Sferruzzi-Perri

Abstract

Previous studies suggest that the placental supply of nutrients to the fetus adapts according to fetal demand. However, the signaling events underlying placental adaptations remain largely unknown. Earlier work in mice has revealed that loss of the phosphoinositide 3-kinase p110α impairs feto-placental growth but placental nutrient supply is adaptively increased. Here we explore the role of p110α in the epiblast-derived (fetal) and trophoblast lineages of the conceptus in relation to feto-placental growth and placental development and transfer function. Using conditional gene manipulations to knock-down p110α either by ~50% or ~100% in the fetal lineages and/or trophoblast, this study shows that p110α in the fetus is essential for prenatal development and a major regulator of placental phenotype in mice. Complete loss of fetal p110α caused embryonic death, whilst heterozygous loss resulted in fetal growth restriction and impaired placental formation and nutrient transport. Loss of trophoblast p110α also resulted in abnormal placental development, although fetuses were viable. However, in response to complete loss of trophoblast p110α, the placenta failed to transport sufficient amino acid to match fetal demands for growth. Usin...Continue Reading

Related Concepts

Body Fluid Compartments
Fetal Growth Retardation
Fetus
Genes
Genetic Engineering
Genome
Laboratory mice
Placenta
Trophoblast
1-Phosphatidylinositol 3-Kinase

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