Mice lacking the orphan receptor Ror1 have distinct skeletal abnormalities and are growth retarded

Natalia Lyashenko, Martina Weissenböck, Amnon Sharir, Reinhold G. Erben, Yasuhiro Minami, Christine Hartmann*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

Ror1 is a member of the Ror-family receptor tyrosine kinases. Ror1 is broadly expressed in various tissues and organs during mouse embryonic development. However, so far little is known about its function. The closely related family member Ror2 was shown to play a crucial role in skeletogenesis and has been shown to act as a co-receptor for Wnt5a mediating non-canonical Wnt-signaling. Previously, it has been shown that during embryonic development Ror1 acts in part redundantly with Ror2 in the skeletal and cardiovascular systems. In this study, we report that loss of the orphan receptor Ror1 results in a variety of phenotypic defects within the skeletal and urogenital systems and that Ror1 mutant mice display a postnatal growth retardation phenotype.

Original languageAmerican English
Pages (from-to)2266-2277
Number of pages12
JournalDevelopmental Dynamics
Volume239
Issue number8
DOIs
StatePublished - Aug 2010
Externally publishedYes

Keywords

  • Mice
  • Postnatal growth retardation phenotype
  • Ror1
  • Skeletal defects

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