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. 2022 May 12;149(9):dev200340. doi: 10.1242/dev.200340

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© 2022. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 5. — Increased severity of limb defects with Prx1-Cre- and Cdx2-Cre-mediated loss of greater numbers of Gpr124 and/or Reck alleles. (A) In Cdx2-Cre;Gpr124^CKO/−;Reck^PW/CKO mice, adult fore feet (left) are essentially unaffected whereas hind feet (right) show digit loss, aberrant structure and ectopic nail-like structures (red arrows). Two views each of one fore foot and two hind feet. (B) A comparison between Cdx2-Cre;Gpr124^CKO/−;Reck^CKO/+ and Cdx2-Cre;Gpr124^CKO/−;Reck^PW/CKO mice at P5 shows the severe hind limb defects caused by replacement of the one remaining WT Reck allele by Reck^PW, which is defective specifically in WNT signaling (white arrows). (C,D) Genetic crosses to remove Gpr124 and/or Reck in the caudal region of the early embryo (Cdx2-Cre) or in the limb mesenchyme (Prx1-Cre). The panels show the number of genotype-of-interest (GOI) progeny obtained relative to the number expected, the percent of progeny with loss of one or more digits (C), and the number of progeny with different numbers of missing digits (D). Parent and progeny genotypes for six crosses (labeled A-F) are shown in C and for two crosses are shown in D. Progeny were scored between P3 and P8.