Plays a role in regulating placenta growth. May act via its PH domain that competes with other PH domain-containing proteins, thereby preventing their binding to membrane lipids. Specifically expressed at high levels in extraembryonic tissues in the developing conceptus (at protein level). Expressed in placenta and yolc sac. Expressed at low levels in fetal liver and kidney. Expressed at high levels in the very early conceptus limited to polar trophectoderm. Strongly expressed in the ectoplacental cone shortly after implantation at 5.5 dpc, and the high expression remains restricted to the extraembryonic tissues at later stages. By 10.5 dpc expression is restricted to the labyrinthine trophoblast and the endodermal component of the visceral yolk sac. Between 12.5 and 14.4 dpc expression in placenta decreases, due to a number of expressing cells. On day 12 of gestation, the abundant expressing cells are trophoblast at the chorionic plate, and clustered type II trophoblast deeper in the labyrinth. Less expressed by terminally differentiated trophoblast. As early as 14.5 dpc, becomes confined to a monolayer of cells at the chorionic plate and to rare cells in septa that protrude into the labyrinth (at protein level). Maternal Phlda2 allele is activated, while paternal Phlda2 is repressed due to genomic imprinting. The PH domain binds phosphoinositides with a broad specificity. It may compete with the PH domain of some other proteins, thereby interfering with their binding to phosphatidylinositol 4,5-bisphosphate (PIP2) and phosphatidylinositol 3,4,5-trisphosphate (PIP3) (By similarity). Mice are viable, and show overgrowth of placentas with expansion of the spongiotrophoblast. These larger placentas do not confer a fetal growth advantage. The Phlda2 locus is imprinted. Loss of imprinting results in overexpression, leading to placental growth retardation phenotypes. Belongs to the PHLDA2 family.