Lasp1 misexpression influences chondrocyte differentiation in the vertebral column
(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:
https://lup.lub.lu.se/record/1489638
- author
- Hermann-Kleiter, Natascha ; Ghaffari-Tabrizi, Nassim ; Blumer, Michael J. F. ; Schwarzer, Christoph ; Mazur, Magdalena LU and Artner, Isabella LU
- organization
- publishing date
- 2009
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Stem Cell and Pancreas Developmental Biology (013212044)
- id
- 2a9b8930-0180-45de-9412-12b95114e6ce (old id 1489638)
- date added to LUP
- 2016-04-01 12:02:44
- date last changed
- 2022-07-22 07:23:08
@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}},
keywords = {{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}},
doi = {{10.1387/ijdb.072435nh}},
volume = {{53}},
year = {{2009}},
}