For example, b-galactosidase protein expression was found in the dorsal aspect of the choroid BEZ235 plexus, whereas the expression of LacZ mRNA is restricted to the rhombic lip. Importantly however, the key b-gal protein expression domains identified mirror those of the LacZ expression. As an independent verification that BAT-gal reporter expression in the developing cerebellum truly indicates Wnt/b-catenin activity we also performed in situ hybridisation for Axin2. Axin2 encodes a negative feedback inhibitor of the Wnt/b-catenin signalling pathway. It is a direct target of TCF/LEF-mediated transcription and is therefore widely used as a readout of Wnt/bcatenin signalling. Within the isthmus and the rhombic lip, the expression of Axin2 closely mirrored both LacZ mRNA expression and b-galactosidase protein expression. However, at E12.5, Axin2 expression was not detected in the anterior portion of the cerebellum immediately below the isthmus. At E12.5 and E14.5, Axin2 showed more diffuse expression in a gradient from both the upper and the lower rhombic lips, compared to both LacZ staining and b-galactosidase protein expression. In this study we have investigated the distribution of Wnt/bcatenin signalling during development of the cerebellum from E12.5 to P21 primarily using the BAT-gal Wnt reporter mouse strain. The specific roles played by Wnt/b-catenin signalling during development of the cerebellum are not yet well characterised. Here, we provide evidence for a specific and dynamic spatio-temporal pattern of Wnt/b-catenin signalling through different stages of cerebellum development. The transcription factor Pax2 is expressed in committed cerebellar interneurons after their exit from the ventricular zone and prior to their terminal differentiation. Thus, colocalisation between Pax2 and b-galactosidase would indicate that committed interneuron progenitors were responding to a Wnt/ b-catenin signal. The pattern of Pax2 expression identified at all three stages analysed was consistent with that expected for interneuron precursors. However, although many b-gal+ and Pax2+ cells were observed in the same cell layers, often in close proximity to each other, no colocalisation was observed in any sections analysed. The b-gal+ cells in the IGL, PCL and ML could also be migratory post-mitotic granule cells, exiting the EGL towards their final destination in the IGL. However, double immunofluorescence between b-galactosidase and NeuN, a marker for postmitotic granule cells, did not reveal any colocalisation of the two proteins in any sections analysed.