The placenta is crucial for the initiation and maintenance of pregnancy. Common complications of human pregnancy, such as preeclampsia, often have unknown etiology but feature contributions from genetic and non-genetic causes. DNA exists in the cell bound by proteins and other molecules, forming a structure known as chromatin. The structural conformation of chromatin is just as important as the DNA code itself, since chromatin structure dictates which components of DNA are active, and therefore able to regulate the cell. Formalin-fixed placentas maintain the structural conformation of their chromatin, making them a uniquely valuable resource to identify the location and activity of regulatory DNA. My proposal seeks to investigate the causes of preeclampsia by comparing the chromatin structure in formalin-fixed placentas from control pregnancies and those complicated with preeclampsia. I will focus on regions of non-coding DNA that regulate gene activity, so-called gene promoters and enhancers, including a special subset of these regions known as transposons. Placental chromatin exhibits a unique structure compared to other tissues, featuring an open conformation around transposons, indicative of their activity in placenta. The activity of gene-regulatory DNA provides the basis of tissue and organ-specific developmental programs. As such, the development and function of the placenta is dictated by the activity of regulatory DNA, and structural variation at these regions can cause disease. I will test the hypothesis that chromatin structure variation of DNA regulatory sequences contributes to the causes of preeclampsia.