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		RESULTS FGF signaling is crucial to proper embryonic development. To determine how interfering with FGF signaling affects 2 day embryos we treated embryos with SU5402, a FGFR inhibitor. The survival ratio for control and experimental embryos was 87% (n=16) and 58% (n=24), respectively, when incubated for 1 day after injection. Interestingly, the experimental embryos exhibited normal limb bud development. However, the craniofacial region of some of the treated embryos were malformed in that they exhibited an abnormal head to body ratio(head being smaller than normal). The most prominent defects were reduced size forebrain, midbrain, and frontal-nasal process (Figure 1). We also observed abnormal blood pools, indicative of poor vascularizaation. The control embryos were developing normally and had no noticeable malformations, when they were observed and photographed (Figure 1). (a) (b) Figure 1. SU5402 treatment. Experimental embryos display delayed development and craniofacial defects. (a) Darkfield images: control- first row, SU5402 - bottom two rows; (b) Digital images: SU5402 - top row, control - bottom row Embryos incubated for 2 days after SU5402 injection showed a 16% (n=12)survival rate. Surviving experimental embryos displayed severe cases of the craniofacial deformities mentioned above as well as extensive blood pooling at the posterior end of the embryos (Figure 2). The survival rate for the control embryos was 86% (n=6). Since SHH and FGF are known to be involved in regulatory feedback loops in the the limb, lung, feather bud and other systems we processed embryos with shh riboprobe to determine the effect of interfering with FGF signaling on levels of shh Figure 2. Comparison of control and SU5402 treated embryos. SU5402 results in decreased hindbrain (HB), midbrain (MB), forebrain (FB), and frontal nasal (FN) processes.