Sdk interacts alternately with Pyd and the WRC to control contact length pulsing. By virtue of tension-dependent localization to vertices and interchangeable interactions with the WRC and Pyd, through the same C-terminal motif, Sdk controls the balance between contraction and expansion of cell contacts that shapes the epithelium of the fly retina. (A) With increasing contraction and tension, Sdk progressively accumulates at vertices. (B) In contracted contacts, actomyosin networks disassemble and Sdk recruits the WRC to promote actin branching and protrusion. (C) With increasing protrusion and contact expansion, levels of Sdk and the WRC decrease at vertices. (D) In expanded contacts, Sdk toggles to interact with Pyd to promote the next contraction. (A) In contracted contacts, Pyd levels decrease again, paving the way for the next expansion. Thus, owing to a dynamic association with vertices and alternating associations with contractile and protrusive effectors, Sdk acts as a tension sensor, transducer, and feedback regulator to modulate cell contact length that shapes the epithelium.