Activated Wnt/β‐catenin signalling is a characteristic of many cancers and drives cell‐cycle progression. Here, we report a mechanism linking Wnt/β‐catenin signalling to centrosome separation. We show that conductin/axin2, a negative regulator of β‐catenin, localizes at the centrosomes by binding to the centriole‐associated component C‐Nap1. Knockout or knockdown of conductin leads to premature centrosome separation—that is, splitting—which is abolished by knockdown of β‐catenin. Conductin promotes phosphorylation of the amino‐terminal serine (Ser 33/37) and threonine (Thr 41) residues of centrosome‐associated β‐catenin. β‐Catenin mutated at these residues causes centrosomal splitting, whereas a phospho‐mimicking mutant of β‐catenin does not. Importantly, β‐catenin‐induced splitting is not inhibited by blocking β‐catenin‐dependent transcription. Treatment with Wnts and inhibition of glycogen synthase kinase 3 block β‐catenin phosphorylation and induce centrosomal splitting. These data indicate that Wnt/β‐catenin signalling and conductin regulate centrosomal cohesion by altering the phosphorylation status of β‐catenin at the centrosomes. Wnt signalling regulates centrosome cohesion. Work by the Behrens group shows that conductin/axin2, a negative regulator of β‐catenin, localizes to centrosomes by binding to the centriole‐associated component C‐Nap1. Conductin/axin2 promotes centrosome cohesion by phosphorylating β‐catenin at centrosomes and the authors propose a model for the regulation of centrosome separation by conductin and Wnt signalling.