The transcription factor CBP, originally identified as a coactivator for CREB^1,2, enhances transcription mediated by many other transcription factors^3–7. Mutations in the human CBP gene are associated with Rubinstein–Taybi syndrome, a haploinsufficiency disorder characterized by abnormal pattern formation⁸, but the mechanism by which decreased CBP levels affect pattern formation is unclear. The hedgehog (hh) signalling pathway is an important determinant of pattern formation, cubitus interruptus (ci), a component in hh signalling, encodes a transcription factor homologous to the Gli family of proteins⁹ and is required for induction of the hh-dependent expression of patched (ptc), decapentaplegic (dpp) and wingless (wg)¹⁰. Haploinsufficiency for the ci-related transcription factor Gli3 causes phenotypic changes in mice (known as 'extra-toes)¹¹ and humans (Greig's cephalopolysyndactyly syndrome)¹² that have similarities to Rubinstein-Taybi syndrome. Here we show that Drosophila CBP (dCBP) functions as a coactivator of Ci, suggesting that the dCBP-Ci interaction may shed light on the contribution of CBP to pattern formation in mammals.