Sulfate is an important nutrient involved in many physiological processes during development, including the biotransformation of steroids and structural proteins, as well as the detoxification of xenobiotics and certain drugs. The fetus, having minimal capacity to produce its own sulfate, is dependent on the mother’s internal sulfate supply which is transported to the fetus via placental sulfate transporters.¹ To date, 10 sulfate transporters have been identified in both the rodent and human genomes. These belong to the solute linked carrier 13 (SLC13) and SLC26 gene families.² Using quantitative real-time PCR (qRT-PCR) and in situ hybridization (ISH) we determined the abundance and spatial localization of all 10 sulfate transporters in both mouse and human placenta. Human placentae (n= 10 male and 6 female) were obtained from uncomplicated healthy pregnancies ≥37 wk gestation at elective caesarean section. Mouse placentas were obtained at embryonic day (E)6.5 to E18.5 gestational ages. qRT-PCR found most sulfate transporters to be expressed throughout pregnancy, however Slc13a4 was the most highly abundant from E12.5 in mouse placenta.³ Slc13a4 mRNA was localised to the syncytiotrophoblast layer of the labyrinth, the site of nutrient exchange in both mouse and human. Based on these findings, we are now investigating an Slc13a4 knockout mouse to study the role of this sulfate transporter in placental and fetal physiology. Heterozygous crosses yielded very small litter sizes (average of 4 pups per litter) and no Slc13a4^-/- mice were born, indicating that loss of Slc13a4 is embryonic lethal. At E14.5 and E16.5, Slc13a4^-/- fetuses exhibit a multitude of developmental phenotypes including oedema and a possible defect in lymphangiogenesis. The current study is providing valuable insight into the critical role of placental sulfate transport during gestation, and how increasing sulfate requirements of the fetus are met by the Slc13a4 sulfate transporter.