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Published on: November 6, 2014
Mice lacking the orphan receptor ror1 have distinct skeletal abnormalities and are growth retarded
Natalia Lyashenko1, Martina Weissenböck, Amnon Sharir
1Institute of Molecular Pathology, 1030 Vienna, Austria.
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.
Insights
Loss of the orphan receptor Ror1 causes skeletal and urogenital defects and postnatal growth retardation in mice. This study investigates the function of Ror1 in embryonic development.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Receptor tyrosine kinases (RTKs) play critical roles in cellular signaling.
- ROR1 (Ror-family receptor tyrosine kinase 1) is broadly expressed during embryonic development, but its functions remain largely uncharacterized.
- Its family member, ROR2, is essential for skeletogenesis and Wnt5a-mediated non-canonical Wnt signaling.
Purpose of the Study:
- To investigate the in vivo function of ROR1 during mouse embryonic development.
- To identify phenotypic consequences of ROR1 loss-of-function.
Main Methods:
- Generation and analysis of ROR1 mutant mice.
- Phenotypic characterization of skeletal and urogenital systems.
- Assessment of postnatal growth.
Main Results:
- ROR1 deficiency leads to significant defects in skeletal and urogenital development.
- ROR1 mutant mice exhibit a pronounced postnatal growth retardation phenotype.
- ROR1 functions in skeletal and cardiovascular systems, partly redundantly with ROR2 during embryogenesis.
Conclusions:
- ROR1 is essential for normal skeletal and urogenital development and postnatal growth.
- ROR1 plays a critical role in embryonic development, with partially overlapping functions with ROR2.
- Further research is needed to elucidate the precise molecular mechanisms underlying ROR1 function.
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