Tubular structures, such as kidney tubules or blood vessels, carry out crucial functions in organisms. Their morphogenesis requires an orchestrated sequence of cellular rearrangements, the disruption of which leads to tubule dysfunction, as observed in polycystic kidney disease. While the initiation of lumen formation is well understood, less is known about the process of lumen expansion. Using time-lapse analysis of the Ciona intestinalis notochord, a simple model of tubulogenesis in which a lumen forms between two cells connected by an apical ring of cell-cell junctions, Di Jiang and co-workers (p. 1639) show that lumen growth is a non-linear process: it exhibits a lag phase, where the lumen continues to grow but the tight junction ring does not expand. These peculiar kinetics are regulated by the contractility and the dynamics of actomyosin filaments at the lateral cell-cell junctions. Mechanistically, TGFβ negatively regulates the enlargement of the tight junction ring through inhibition of the RhoA-ROCK pathway, which reduces actomyosin contractility. After the lag phase, the osmotic pressure created in the lumen by the apically localised anion transporter Slc26 allows the enlargement of the junctional ring to resume. This study reveals unexpected and complex lumen expansion kinetics, furthering our knowledge of tubule morphogenesis.