The Objective

Understanding the basic molecular mechanisms for growth in utero will eventually lead to prevention or therapy for intrauterine growth restriction (IUGR). Our group and others have shown that imprinted genes have an important role in fetal growth both in mouse and man (1). Some of these genes are imprinted in the placenta and their role appears to be linked to successful nutrient transfer, which is vital for normal fetal growth (2). The objective of this proposal is to follow up our study on the maternally expressed PHLDA2 imprinted gene and its promoter region. The expression of PHLDA2 in the placenta has been negatively correlated with growth (3). Recently we have found a deletion polymorphism in the PHLDA2 promoter region that exhibits a trend implicating a role in its growth suppressing function.