Female reproductive tract (FRT) development in vertebrates is controlled by Wnts, but little is known about the different intracellular pathways involved. Now, Alysia vandenBerg and David Sassoon describe how non-canonical Wnt signalling through a core member of the planar cell polarity (PCP) signalling pathway, vang-like 2 (Vangl2), is involved in this process(p. 1559). They report that loop-tail mice, which carry a Vangl2 mutation(Vangl2Lp), have FRT defects at birth that resemble those of Wnt7a mutants. Their findings show that the polarity of uterine epithelial cells in Vangl2Lp mice is abnormal, with defective cytoskeletal actin polarisation and mislocalised scribble 1 - an apicobasal polarity protein. As Vangl2Lp mutants die at birth, the researchers grafted FRTs from mutants into normal mice to study the later effects of this mutation. They found that the initial defects worsen over two weeks and that Wnt7a levels are reduced in both homozygous and heterozygous grafted Vangl2Lp FRTs, indicating that Vangl2 acts dominantly in the FRT. From their findings, the authors conclude that both canonical and non-canonical Wnt signalling participate in FRT development.