Obesity develops due to an imbalance of increased energy intake over decreased energy expenditure. A sedentary lifestyle in combination with readily available, energy-dense food sources have led to a pandemic spread of obesity in modern societies that represents a significant challenge to medical care systems. Excess calories from food are stored as triglycerides within the white adipose tissue (WAT), exacerbating a number of diseases associated with pathological overweight, such as diabetes, cardiovascular complications, and dyslipidaemias. Brown adipose tissue (BAT) is a specialized fat tissue that is dedicated to body temperature regulation. Due to its remarkable capacity for thermogenesis and its demonstrated presence in adult humans, BAT holds great promise for the treatment of obesity and the metabolic syndrome [1]. Two distinct types of brown fat cells have recently been described in mammalians: the constitutive or classical BAT (cBAT), which is of embryonic origin and anatomically located in the interscapular region of mice; and the so called recruitable BAT (rBAT), that has alternatively been termed brite (brown-in-white) or beige fat, due to its predominant anatomical distribution within WAT. While a common set of progenitor cells may give rise to white adipocytes and rBAT (within WAT), cBAT derives from a developmental lineage that is more closely related to skeletal muscle. Accordingly, recent findings have not only established that cBAT-progenitors are marked by a myogenic gene expression signature, but also that myogenic transcription factors, such as Myf5 and Pax7, are expressed in a common lineage of embryonic progenitors that give rise to cBAT in addition to skeletal muscle [2-4]. Morphogens have been implicated as instructive signals in the lineage determination of brown adipogenic progenitors. In this line, we were recently able to show that bone morphogenetic protein (BMP)-7 regulates the formation of brown adipocytes in multipotent progenitor cells, whereas loss of BMP7 resulted in a marked paucity of embryonic cBAT [5]. Interestingly, emerging evidence has also implicated BMP7 and BMP8b in the control of thermogenic capacity of mature BAT, altogether highlighting the central role of this pathway in brown fat physiology. Taking advantage of these observations, we generated a knock-out mouse model with conditional ablation of the type 1A BMP receptor, BMPR1A, which functions as a major receptor for BMP7. Loss of BMPR1A in cells of the common muscle/cBAT-lineage severely impairs the formation of cBAT but not skeletal muscle during embryogenesis, thereby leading to reduced body temperature in new-born mice. Adult knockout mice, however, display an unexpected normalization of body temperature and overall thermogenic capacity. Importantly, knockouts are able to resume normal body temperature following prolonged exposure to cold, indicating that compensatory mechanisms are in place to counter the defect in thermoregulation induced by cBAT-paucity. Indeed, knockout mice show a greater propensity to recruit brown adipocytes within their classical WAT-depots, a process that is associated with increased sympathetic input to WAT. This previously unknown compensatory mechanism, aimed at restoring total brown-fat-mediated thermogenic capacity in the body, is sufficient to maintain normal temperature homeostasis and resistance to diet-induced obesity. These data suggest an important physiological cross-talk between constitutive and recruitable brown adipocytes involving cBAT-to-brain and brain-to-WAT communications and that is at least partially mediated by the sympathetic nervous system. This regulatory mechanism of body temperature may participate in the control of energy balance and metabolic disease and could provide a novel target for therapeutic approaches aimed at shifting the energy balance to a beneficial proportion [6].