Fig. 1. Abnormalities found in chimeras, heterozygous, and homozygous null embryos.

BMP2 chimeras (A-E) were generated from null ES cells carrying the LacZ gene and wild type blastocysts and were harvested at E9.5. Shown are different levels of contribution of null ES cells to chimeric development in increasing amounts from A to E. X-gal stains null ES cells blue. Note that defects appear at fairly low levels of contribution. Black arrowheads show defects of the cephalic region and grey arrowheads show other stage-specific developmental defects. A. No contribution chimera shows no apparent defects. B. Low contribution chimera has an abnormal shaped head and fails to form telencephalic vesicles. C. Middle contribution chimera shows postneurulation (closed neural tube) defects in the forebrain, midbrain, and hindbrain regions of the developing embryo. The heart has not looped properly. D. High contribution chimera has open neural tube defects as well as stalled development in the anterior and posterior portions of the embryo. There is also abnormal heart looping, a failure to develop limb buds and failure of embryonic turning. E. Very high contribution chimera fails to develop any normal structures including somites. BMP2 Heterozygous and Homozygous Null Embryos, E9.5. White arrowheads show cephalic defects while grey arrowheads show other stage-specific developmental defects. Defects occur in some heterozygous embryos, (F-J) where postneurulation defects show abnormal head shape and lack of telencephalic vesicles (F) or embryos have open NT defects in the forebrain region (G, H) or forebrain-midbrain region, while some have completely open NT in the cephalic region (J). For homozygous nulls (K-O), defects in the developing embryo include failure to close the NT, abnormal heart development, lack of limb bud development and also failure to turn. Scale bar =1mm