Skeletal defects in ringelschwanz mutant mice reveal that Lrp6 is required for proper somitogenesis and osteogenesis.

@article{Kokubu2004SkeletalDI,
  title={Skeletal defects in ringelschwanz mutant mice reveal that Lrp6 is required for proper somitogenesis and osteogenesis.},
  author={Chikara Kokubu and Ulrich Heinzmann and Tomoko Kokubu and Norio Sakai and Takuo Kubota and Masanobu Kawai and Matthias B. Wahl and Juan Galceran and Rudolf Grosschedl and Keiichi Ozono and Kenji Imai},
  journal={Development},
  year={2004},
  volume={131 21},
  pages={5469-80}
}
Here, we present evidence that Lrp6, a coreceptor for Wnt ligands, is required for the normal formation of somites and bones. By positional cloning, we demonstrate that a novel spontaneous mutation ringelschwanz (rs) in the mouse is caused by a point mutation in Lrp6, leading to an amino acid substitution of tryptophan for the evolutionarily conserved residue arginine at codon 886 (R886W). We show that rs is a hypomorphic Lrp6 allele by a genetic complementation test with Lrp6-null mice, and… CONTINUE READING