The loss of two regulatory RNAs is critical for the development of Prader-Willi syndrome. One of these RNAs prevents the formation of a truncated serotonin receptor. We will test the role of this truncated serotonin receptor in the production of growth hormones and determine whether it is a 'master regulator' for other receptors. Based on our preliminary studies and published literature, it is likely that the truncated receptor sequesters other receptors inside the cell, which prevents the production of growth hormone. This idea will be tested in cells and in mouse models. Importantly, we will determine weather a short synthetic RNA promotes growth hormone production and could substitute one of the missing regulatory RNAs.