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Isabella Artner

Research team manager

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Lasp1 misexpression influences chondrocyte differentiation in the vertebral column

Author

  • Natascha Hermann-Kleiter
  • Nassim Ghaffari-Tabrizi
  • Michael J. F. Blumer
  • Christoph Schwarzer
  • Magdalena Mazur
  • Isabella Artner

Summary, in English

The mouse mutant wavy tail Tg(Col1a1-lacZ)304ng was created through transgene insertion and exhibits defects of the vertebral column. Homozygous mutant animals have compressed tail vertebrae and wedge-shaped intervertebral discs, resulting in a meandering tail. Delayed closure of lumbar neural arches and lack of processus spinosi have been observed; these defects become most prominent during the transition from cartilage to bone. The spina bifida was resistant to folic acid treatment, while retinoic acid administration caused severe skeletal defects in the mutant, but none in wild type control animals. The transgene integrated at chromosome 11 band D, in an area of high gene density. The insertion site was located between the transcription start sites of the RpI23 and Lasp1 genes. LASP1 (an actin binding protein involved in cell migration and survival) was found to be produced in resting and hypertrophic chondrocytes in the vertebrae. In mutant vertebrae, temporal and spatial misexpression of Lasp1 was observed, indicating that alterations in Lasp1 transcription are most likely responsible for the observed phenotype. These data reveal a yet unappreciated role of Lasp1 in chondrocyte differentiation during cartilage to bone transition.

Department/s

  • Stem Cell Center

Publishing year

2009

Language

English

Pages

983-991

Publication/Series

International Journal of Developmental Biology

Volume

53

Issue

7

Document type

Journal article

Publisher

U B C Press

Topic

  • Cell and Molecular Biology

Keywords

  • folic acid
  • transgene insertion
  • cartilage bone transition
  • retinoic
  • acid
  • collagen

Status

Published

ISBN/ISSN/Other

  • ISSN: 1696-3547