Neurogenesis changes β-catenin shipping address from adherens junctions to nucleus to booster axonal growth.

Here we show that in the developing spinal cord (SC), after the early Wnt-mediated Tcf-transcription activation that confers dorsal identity to neural stem cells (NSCs), neurogenesis readdressed β-catenin from the adherens junctions (AJs) to the nucleus to stimulate Tcf-dependent transcription in a Wnt-independent manner. This new β-catenin activity regulates genes implicated in several aspects of contralateral axon growth, including axon guidance and adhesion. Using live imaging of ex-vivo chick neural tube (NT), we show that the nuclear accumulation of β-catenin and the rise of Tcf-dependent transcription both initiate before the dismantling of the AJs, and remain during the axon elongation process. Notably, we demonstrate β-catenin activity in post-mitotic cells depends on TCF7L2 and is central for spinal commissural axon growth. Together, our results reveal a Wnt independent Tcf/β-catenin regulation of genes that control the growth and guidance of commissural axons in chick SC.