Muscle β-catenin has been shown to play a role in the formation of the neuromuscular junction (NMJ). Our previous studies showed that muscle-specific conditional knockout of β-catenin (HSA-β-cat−/−) results in early postnatal death in mice. To understand the underlying mechanisms, we investigated the electrophysiological properties of muscle cells from HSA-β-cat−/− and control mice, and found that, in the absence of muscle β-catenin, the resting membrane potential (RMP) depolarised in muscle cells from the diaphragm, gastrocnemius and extensor digitorum longus muscles. Furthermore, in a primary line of mouse myoblasts (C2C12 cells) transfected with small-interfering RNAs targeting β-catenin, the RMP was depolarised as well. Finally, the expression levels of the α2 subunit of sodium/potassium adenosine triphosphatase were reduced by β-catenin knockdown in vitro or deletion in vivo. These results suggest a possible mechanism underlying the depolarised RMP in the absence of muscle β-catenin, and provide additional evidence supporting a role for β-catenin in the development of NMJs.
We recorded depolarisation in skeletal muscle cells with β-catenin conditionally deleted both in vivo and in vitro. In addition, we found that the expression levels of the α2 subunit of Na,K adenosine triphosphatase were reduced by either knockdown of β-catenin in vitro or its deletion in vivo. These results suggest that β-catenin plays a role in regulating the resting membrane potential of the postsynaptic apparatus at the vertebrate neuromuscular junction.