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. Author manuscript; available in PMC: 2024 Apr 24.
Published in final edited form as: Curr Top Dev Biol. 2023 Mar 17;153:195–227. doi: 10.1016/bs.ctdb.2023.01.009

Figure 2. Robinow syndrome and Robinow-like disorders arise from mutations in components of WNT5A-ROR signaling.

Figure 2.

(A) Wnt5a knockout mouse embryos (E18.5, images from (Yamaguchi et al., 1999)) exhibit body axis, limb, and tail truncations in addition to underdeveloped external genitalia and craniofacial malformations, compared to their wild-type littermates. These physical features are phenocopied in Ror2 knockout mouse embryos (B; E12.5 embryos derived from previously described Wnt5a (Yamaguchi et al., 1999) and Ror2 (Ho et al., 2012) mutant lines, photographed by S. Srinivasan. Scale bar = 1mm), as well as in RS patients (C; image from (Person et al., 2010), photographed by J. Lohr) and bulldogs (C; French bulldog).