--- - |2+ Key points summary Exogenous NHE1 expression stimulated collective migration of epithelial cell sheets Stimulation with epidermal growth factor (EGF), a key morphogen, primarily increased migration of the front row of cells, whereas NHE1 increased that of submarginal cell rows, and the two stimuli were additive Accordingly, NHE1 localized not only to the leading edges of leader cells, but also in cryptic lamellipodia in submarginal cell rows NHE1 expression disrupted the morphology of epithelial cell sheets and 3D cysts Abstract Collective cell migration plays essential roles in embryonic development, in normal epithelial repair processes, and in many diseases including cancer. The Na+/H+ Exchanger 1 (NHE1, SLC9A1) is an important regulator of motility in many cells and has been widely studied for its roles in cancer, yet its possible role in collective migration of normal epithelial cells has remained unresolved. Here, we show that NHE1 expression in MDCK‐II kidney epithelial cells accelerated collective cell migration. NHE1 localized to the leading edges of leader cells, as well as to cryptic lamellipodia in submarginal cell rows. Epidermal growth factor (EGF), a kidney morphogen, increased displacement of the front row of collectively migrating cells and reduced the number of migration fingers. NHE1 expression increased number of migration fingers and increased displacement of submarginal cell rows, resulting in additive effects of NHE1 and EGF. Finally, NHE1 expression resulted in disorganized development of MDCK‐II cell cysts. Thus, NHE1 contributes to collective migration and epithelial morphogenesis, suggesting roles for the transporter in embryonic and early postnatal development. This article is protected by copyright. All rights reserved - 'The Journal of Physiology, Volume 0, Issue ja, -Not available-. '