Satellite cells are the resident stem cells of skeletal muscle. Upon receiving cues from their myofibre-adjacent niche, activated satellite cells undergo asymmetric division to generate a transit amplifying population called myoblasts, as well as to replenish the satellite cell pool. Wnts are key signals that control both satellite cell and myoblast behaviour. The central effectors of the canonical Wnt signalling pathway are TCF/LEF factors and beta-catenin that together bind to Wnt target genes and transduce transcriptional responses. The homeobox protein Barx2 is expressed in satellite cells and myoblasts and analysis of Barx2 null mice shows its critical role in muscle growth and repair. We previously reported the novel finding that Barx2, the satellite cell marker Pax7, and muscle regulatory factors (MRFs) such as MyoD, interact with the core Wnt effector complex to regulate a Wnt reporter gene. We now show that expression of Barx2 in myoblasts regulates endogenous canonical Wnt target genes Axin2 and CyclinD1. Activation of these genes involves proximal promoter regions containing one or more TCF/LEF sites. Promoter constructs are activated by both beta-catenin and Barx2, whilst dominant negative TCF and Pax7 suppress this activation. Mutation of the promoter TCF/LEF elements disrupts beta-catenin- and Barx2-mediated activation, consistent with observations that Barx2 interacts with beta-catenin and TCF4 and is recruited to TCF/LEF sites. Characterization of primary myoblasts from wildtype and Barx2-null mice reveals that Barx2 expression is induced by Wnt ligands, and that loss of Barx2 downregulates canonical Wnt targets. These data suggest a positive feed-forward loop between Barx2 and Wnt signalling. Taken together with our previous work, our new findings support a model in which Barx2 and MyoD are key mediators of Wnt-driven myoblast expansion and differentiation (myogenesis), while Pax7 antagonizes this function consistent with its role in promoting long-term satellite cell self-renewal.