Our laboratory investigates mechanisms that regulate embryonic development. We have a long-standing interest in understanding how signaling centers that are established during development operate to subdivide organ primordia into distinct functional units. More recently, we began to investigate mechanisms that drive epithelial morphogenesis at later developmental stages. We identified new roles for the WAVE regulatory complex (WRC), the Arp2/3 complex and F-actin branching in epithelial remodeling. Our work suggests that pushing forces generated by F-actin branching coordinate with pulling forces generated by contractile actomyosin networks to enable epithelial tissues to undergo robust remodeling while maintaining epithelial integrity. To better understand how pushing forces contribute to epithelial remodeling, the objective of our current studies is to determine how the WRC is targeted to the cell surface, how it is activated and inactivated dynamically and how protrusive branched actin networks coordinate with contractile actomyosin networks to control epithelial remodeling. Insights gained from these studies will apply generally to the understanding of epithelial morphogenesis, congenital disease and pathologies such as cancer that disrupt epithelial organization.