Loss of Inverted Formin-2 impairs intracellular trafficking and trophoblast invasion, resulting in maternal hypertension and intrauterine growth restriction, which represents a novel model of impaired placental invasion that encompasses critical aspects of the great obstetrical syndromes.

Investigation of mouse models from forward mutagenetic screen reveals that the gene Spag7 is essential for embryonic development and energy homeostasis later in life.

Fetus and trophoblast interplay to regulate fetal nutrient supply and, ultimately, affect healthy growth.

Growth-delayed offspring generated from eggs that lacked normal epigenetic programming exhibited a remarkable capacity to undergo late gestational fetal growth recovery, despite inefficient placental function.

Expression of Bisphosphoglycerate mutase, a key enzyme affecting the release of oxygen from hemoglobin, is augmented in the murine placenta challenged by gestational hypoxia in mice while its expression is attenuated in placenta of human FGR.

Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

Mineralized placental tissue from Late Byzantine Troy enables the detailed reconstruction of genomes of mixed bacterial species responsible for maternal sepsis in the ancient world.

VE-cadherin is required for trophoblast invasion of the maternal decidua and spiral arteries.

The role of placental aging and metabolic stress in driving labor onset is demonstrated, with a novel mouse model of preterm labor in which injection of a prolyl hydroxylase inhibitor stabilizes placental hypoxia-inducible factor 1 and significantly shortens gestational length.