The APC gene codes for a large protein with multiple cellular functions and interactions (Fodde et al., 2001a; McCartney and Näthke, 2008; Nelson and Näthke, 2013). APC is an essential component of the canonical Wnt signaling pathway and is required for the formation of a cytoplasmic complex that targets ß-catenin for proteasomal degradation when Wnt signals are absent (Clevers and Nusse, 2012). APC also participates in several cellular processes: cell adhesion and migration (Watanabe et al., 2004), actin dynamics (Moseley et al., 2007), and chromosome segregation (Fodde et al., 2001b). In humans, APC mutations lead to the second most common cause of cancer death (Mori n et al., 1997). More specifically, in high turnover tissues, such as in the intestine, loss or mutation of APC leads to uncontrolled proliferation and accumulation of aberrant cells, thereby leading to carcinogenesis (Sansom et al., 2004; Andreu et al., 2005). Due to its role in controlling cell cycle progression of several stem cell compartments, APC was a good candidate to regulate muscle stem cell proliferation and quiescence, which to date are poorly characterized.

In adult skeletal muscle, a tissue with slow turnover, a pool of Pax7+ muscle stem cells called satellite cells ensures myofibers regeneration after injury (Seale et al., 2000; Lepper et al., 2011; Günther et al., 2013). Satellite cells are quiescent and lie under the basal lamina of their host muscle fibers unless