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  Cloning and expression pattern of chicken Ror2 and functional characterization of truncating mutations in Brachydactyly type B and Robinow syndrome

Stricker, S., Van Wijk, N. V., Witte, F., Brieske, N., Seidel, K., & Mundlos, S. (2006). Cloning and expression pattern of chicken Ror2 and functional characterization of truncating mutations in Brachydactyly type B and Robinow syndrome. Developmental Dynamics, 235(12), 3456-3465. doi:10.1002/dvdy.20993.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-8327-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-8328-A
Genre: Journal Article
Alternative Title : Dev Dyn

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 Creators:
Stricker, Sigmar1, Author              
Van Wijk, Nicole Verhey2, Author
Witte, Florian3, Author              
Brieske, Norbert1, Author              
Seidel, Kathrin2, Author
Mundlos, Stefan1, Author              
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              
2Max Planck Society, ou_persistent13              
3Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433547              

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Free keywords: Ror2; Brachydactyly; Robinow syndrome; limb development; cartilage; chicken
 Abstract: Ror2 is a receptor tyrosine kinase mutated in the human syndromes Brachydactyly type B (BDB) and recessive Robinow syndrome (RS). In this study, we used the chick as a model to investigate the role of Ror2 in skeletogenesis and to elucidate the functional consequences of Ror2 mutations. For this purpose, we cloned chicken Ror2 and analyzed its expression pattern at various embryonic stages by in situ hybridization and immunolabeling. We document expression of cRor2 in several organs, including mesonephros, heart, nervous system, intestine and cartilage. The high conservation of expression when compared with the mouse underlines the validity of the chick as a model system. Using replication-competent retroviral vector-mediated overexpression, we analyzed the functional consequences of truncating BDB and RS mutations in the developing chick limb. Overexpression of Ror2 mutants led to a disturbance of growth plate architecture and a severe block of chondrocyte differentiation, demonstrating the functional importance of Ror2 in skeletogenesis.

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Language(s): eng - English
 Dates: 2006-12
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: eDoc: 313092
DOI: 10.1002/dvdy.20993
 Degree: -

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Title: Developmental Dynamics
  Alternative Title : Dev Dyn
Source Genre: Journal
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Pages: - Volume / Issue: 235 (12) Sequence Number: - Start / End Page: 3456 - 3465 Identifier: ISSN: 1058-8388