Actin is an integral component of the apical junction of epithelial cells. However, the function of the branched actin network at apical junctions is still not clear. We have conducted genetic screens for the essential regulators of cell migrations during C. elegans embryonic morphogenesis and identified a pathway that includes the GTPase Rac1/CED-10, the WAVE/SCAR/GEX complex and the Arp2/3 complex. Consequently we have shown that these branched actin regulators promote enrichment of membrane proteins required for apical junction development in C. elegans epithelia. We therefore investigated how Arp2/3 and its WAVE/SCAR nucleation promoting factor help build and maintain apical junctions. TEM studies showed that depletion of WAVE/SCAR components post-embryonically results in reduced size of adherens junctions. This is similar to the effects of depleting either of two C. elegans apical junction complexes, the Cadherin Complex or the DLG-1/AJM-1 Complex. Live imaging in embryos showed that WAVE/SCAR and both of these C. elegans apical junction complexes promote F-actin accumulation at the apical junction. Accumulation of alpha-catenin/HMP-1, the Cadherin Complex component that binds F-actin, is greatly altered in embryos depleted of WAVE components. Further, WAVE can immunoprecipitate alpha-catenin/HMP-1 and DLG-1/Discs Large, components of two C. elegans apical junction complexes. Our studies suggest that distinct C. elegans apical junction complexes help recruit WAVE/SCAR, which in turn leads to the enrichment and retention of alpha-catenin at the apical junction, resulting in robust apical actin accumulation.