The rotation of cilia on cells within the node of mammalian embryos generates a leftward fluid flow that establishes left-right asymmetry. But what regulates ciliogenesis at the node? Here (p. 3915), Yuji Mishina and colleagues show that cell cycle arrest, mediated by bone morphogenetic protein (BMP) signalling, is required in node cells to trigger nodal ciliogenesis in mice. The authors show that epiblast-specific deletion of Acvr1, which encodes a BMP type 1 receptor, results in abnormal left-right patterning in early embryos; the node forms in these mutants but nodal ciliogenesis is compromised. Using Acvr1-deficient mouse embryonic fibroblasts, they further demonstrate that BMP signalling through ACVR1 positively regulates p27Kip1 stability and phosphorylation, which in turn maintains quiescence and allows the formation of primary cilia. Importantly, the researchers report, p27Kip1 is present and phosphorylated in quiescent nodal cells, whereas the corresponding cells in Acvr1 mutants are proliferative and show reduced p27Kip1 expression and phosphorylation. These studies provide valuable insight into the mechanisms by which primary cilia form at the node.