Advanced

Lasp1 misexpression influences chondrocyte differentiation in the vertebral column

Hermann-Kleiter, Natascha; Ghaffari-Tabrizi, Nassim; Blumer, Michael J. F.; Schwarzer, Christoph; Mazur, Magdalena LU and Artner, Isabella LU (2009) In International Journal of Developmental Biology 53(7). p.983-991
Abstract
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... (More)
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. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
folic acid, transgene insertion, cartilage bone transition, retinoic, acid, collagen
in
International Journal of Developmental Biology
volume
53
issue
7
pages
983 - 991
publisher
U B C Press
external identifiers
  • wos:000270244400009
  • scopus:70350034160
ISSN
1696-3547
DOI
10.1387/ijdb.072435nh
language
English
LU publication?
yes
id
2a9b8930-0180-45de-9412-12b95114e6ce (old id 1489638)
date added to LUP
2009-10-21 17:03:23
date last changed
2017-01-01 04:47:05
@article{2a9b8930-0180-45de-9412-12b95114e6ce,
  abstract     = {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.},
  author       = {Hermann-Kleiter, Natascha and Ghaffari-Tabrizi, Nassim and Blumer, Michael J. F. and Schwarzer, Christoph and Mazur, Magdalena and Artner, Isabella},
  issn         = {1696-3547},
  keyword      = {folic acid,transgene insertion,cartilage bone transition,retinoic,acid,collagen},
  language     = {eng},
  number       = {7},
  pages        = {983--991},
  publisher    = {U B C Press},
  series       = {International Journal of Developmental Biology},
  title        = {Lasp1 misexpression influences chondrocyte differentiation in the vertebral column},
  url          = {http://dx.doi.org/10.1387/ijdb.072435nh},
  volume       = {53},
  year         = {2009},
}