Several members of the transforming growth factor-b (TGF-b) family including growth and differentiation factors -8 and -11 (GDF8 and GDF11), the activins, and bone morphogenetic proteins (BMPs) play essential roles in the regulation of muscle homeostasis. We identified a novel TGF-b type III-like receptor present in skeletal muscle that binds select TGF-b ligands. Here, we examined if and how the receptor modulates TGF-b signalling. In heterologous HEK293 cells, GDF8 and GDF11-stimulated SMAD2 phosphorylation was significantly reduced (-36% and -48% respectively) upon ectopic expression of the receptor. As these ligands regulate muscle physiology, we next examined the effects of receptor over-expression in mice. An adeno-associated viral vector (AAV) expressing the receptor (AAV:receptor) or control AAV (AAV:iRFP) was administered (1x109-5x109vg) to the tibialis anterior (TA) muscles of 8-week old healthy male wild-type C57BL/6J mice. At 4-weeks post injection, TAs were harvested for histological and molecular assessment. TAs injected with AAV:receptor were on average significantly reduced in mass relative to the TAs injected with control AAV:iRFP (-8.4%, n=5, *p<0.05) owing to muscle fibre atrophy. Receptor over-expression suppressed the BMP-driven SMAD1/5/8 signalling pathway whilst simultaneously upregulating the SMAD2/3 pathway to trigger an atrophic response in muscle, as assessed by western blot analysis of TA muscle protein lysates. Collectively, the findings indicate that overexpression of the novel type III-like receptor in muscle may promote atrophy via modulation of TGF-b signalling. As the receptor is present in skeletal muscle, our findings suggest that it may act as physiological regulator of muscle homeostasis via interactions with select TGF-b ligands.