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 belonging to the solute linked carrier 13 (SLC13) and SLC26 gene families.² Recently we have identified the Slc13a4 sulfate transporter to be the most highly abundant sulfate transporter from E12.5 in mouse placenta³ and mRNA was localized to the syncytiotrophoblast layer of the labyrinth, the site of nutrient exchange in both mouse and human.⁴ 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. Our findings so far have indicated that a loss of Slc13a4 is embryonic lethal due to a multitude of pronounced developmental phenotypes including skeletal underdevelopment, 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.