Collective cell migration (CCM) drives physiological processes such as embryogenesis, vascular sprouting, and wound healing, but is also a major contributor to cancer metastasis. Ras homolog family member A (RhoA) drives CCM by modulating actomyosin cytoskeletal activity. RhoA activity is tightly spatiotemporally controlled during CCM, but whether these activation dynamics are shared by its downstream effectors is unknown. To investigate the role of RhoA's downstream effector Rho-associated kinase (ROCK) in stationary and collectively migrating fibroblasts, we developed a new single-color FRET-based ROCK sensor, the Rho Kinase Activity Reporter (RhoKAR) sensor. We observed calcium-dependent activation of ROCK using the RhoKAR sensor following ionomycin stimulation. With modified scratch assays that we developed, we quantified ROCK activity in parallel with CCM. Scratch wounding caused an increase in ROCK activity. We also observed blunting of CCM in response to pharmacological inhibition of ROCK or depletion of intracellular calcium with EGTA. To study the role of calcium from different sources in driving ROCK activity during CCM, we applied carbenoxolone, a gap junction blocker, to collectively migrating fibroblasts. Carbenoxolone decreased ROCK activity and intracellular calcium at corresponding time points and slowed CCM. These results indicate that gap junction-mediated intercellular calcium signaling drives ROCK activity during collective cell migration.