Schematic illustration of BMP activity in embryos carrying wild type or mutant alleles of Bmp2, 4 and/or 7. In the hypothetical model, class I/II heterodimers form preferentially. In addition, it is hypothesized that there is an excess of class II BMPs that form homodimers in the wild type condition but are available to form heterodimers to compensate for loss of any single class II BMP. In embryos lacking a single copy of Bmp2 or Bmp4, activity contributed by the heterodimer pool is reduced but there is no further reduction in heterodimers when a single copy of Bmp7 is also removed, due to redundancy with other Class II BMPs. A fraction of the heterodimer pool is inactivated in Bmp7R-GFlag heterozygotes and additional removal of a single copy of Bmp2 or Bmp4 further depletes the heterodimer pool. (A–E’) Photographs of E14.5 wild type and mutant littermates (A–E) and corresponding hematoxylin and eosin stained transverse sections through the abdomen (A’-E’; approximate position of section indicated by the black bar in A-E). Arrows indicated externalized viscera (D, D’, E) and arrowheads denote peripheral edema (D, D’, E, E’). (F–H’) Ventral views of hearts dissected from E15.5 Bmp7R-GFlag/+ (F) or Bmp7R-GFlag/+;Bmp2-/+ embryos (G–H) and corresponding hematoxylin and eosin stained coronal sections (F’–H’). Asterisks denote VSDs (G’, H’), arrow indicates abnormal positioning of the aorta exiting the right ventricle (H’), arrowheads indicate thin, non-compacted ventricular wall (G’). (I–P’) Expression of Nkx2.5 was analyzed by whole mount in situ hybridization in littermates generated by intercrossing Bmp4-/+ and Bmp7R-GFlag/+ (I–L’) or Bmp7-/+ and Bmp7R-GFlag/+ mice (M–P’). Photographs of intact embryos at E10.5 (I–P) and photographs of hearts dissected from corresponding embryos (I’–P’) are shown. RA; right atrium, LA; left atrium, CA; common atrium, RV; right ventricle, LV; left ventricle, OFT; outflow tract. The OFT is outlined in I’, L’, M’ and P’. Scale bars in all panels correspond to 1 mm.