Obesity represents a severe challenge to medical care systems worldwide. Adequate treatment strategies are urgently needed to counter not only pathological overweight but also its associated complications such as diabetes and cardiovascular disease. Brown adipose tissue (BAT) dissipates energy in the form of heat and has therefore been proposed as a target for anti-obesity therapies. Recently, it has become clear that metabolically active brown fat cells can be observed in adult humans, thus supporting the notion of a viable treatment approach for obesity by targeting BAT (Nedergaard et al., 2007). Two types of brown adipose tissue can be found in mice and in all likelihood also in human subjects (Cypess et al., 2013): The classical brown adipose tissue that develops during embryogenesis and that persists throughout life and, secondly, the brite (brown-in-white) adipocytes that are recruited either through transdifferentiation of mature white adipocytes or through differentiation of progenitor cells present in white adipose tissue depots. Previous studies have shown that these two tissue types arise from distinct developmental origins, altogether suggesting that classical brown adipocytes are more closely related the myogenic satellite cells of the muscle lineage than to white adipogenic progenitors (Seale et al., 2008). We and others recently demonstrated that bone morphogenetic protein (BMP)-7 and other BMPs play an important role in brown adipogenesis (Tseng et al., 2008; Schulz et al., 2013b). Specifically, BMP-signalling has been implicated in the process of brown adipogenic lineage determination and differentiation as well as on the systemic level where BMPs affect thermogenesis and the sympathetic activation of brown adipocytes. To determine the role of BMPR1A in brown fat development, we generated a mouse model in which BMPR1A is deleted in classical brown adipocyte progenitor cells using the Cre/loxP system (Schulz et al., 2013a). Interscapular brown fat mass was significantly reduced in knockout (KO) mice whereas skeletal muscle that arises from the same cellular lineage appeared essentially normal. As a result of loss of classical brown adipose tissue, a compensatory browning of white adipose tissue depots was observed that was mostly due to increase sympathetic input to white fat. Of note, compensatory browning not only led to a full recovery of thermogenesis in the knockout mice but also led to improved insulin sensitivity suggesting that brite adipocytes might possess additional metabolic benefits. In summary, these findings establish an essential role of BMP signalling network in the development of brown fat depots and suggest that targeting BMP signalling may present a strategy to counteract obesity by increasing brown fat mass and function.