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Journal of Heredity Advance Access originally published online on August 28, 2007
Journal of Heredity 2007 98(6):575-580; doi:10.1093/jhered/esm065
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© The American Genetic Association. 2007. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Short-Limbed Dwarfism: slw Is a New Allele of Npr2 Causing Chondrodysplasia

Chizuru Sogawa, Takehito Tsuji, Yusuke Shinkai, Kentaro Katayama, and Tetsuo Kunieda

From the Graduate School of Natural Science and Technology, Okayama University, Tsushima-naka, Okayama 700-8530, Japan (Sogawa, Tsuji, Shinkai, Katayama, and Kunieda). Chizuru Sogawa is now at the National Institute of Radiological Sciences, Inage, Chiba 263-8555, Japan; and Yusuke Shinkai is now at the Research Center for Health Science of Nanoparticles, Tokyo University of Science, Noda, Chiba 278-8510, Japan

Address correspondence to T. Tsuji at the address above, or e-mail: takehito{at}cc.okayama-u.ac.jp.

Short-limbed dwarfism (SLW) is a new mutant mouse characterized by a dwarf phenotype with markedly short body, limbs, and tail. In the present study, we investigated the skeletal phenotypes of the SLW mouse and determined the chromosomal localization to identify the gene responsible for the phenotypes (slw). Skeletal preparations stained with alcian blue and alizarin red revealed that longitudinal growth of the extremities of the affected (slw/slw) mice was significantly reduced in comparison with that of normal mice, whereas the positions and numbers of skeletal elements were normal. Histological examination of tibial growth plates of the affected mice showed that the numbers of proliferating and hypertrophic chondrocytes were obviously diminished. These phenotypes resembled to those of human chondrodysplasias caused by defective chondrocyte proliferation and differentiation. We mapped the slw locus on an 11.7-cM interval of the proximal region of mouse chromosome 4 by linkage analysis. Furthermore, allelism test using Npr2cn locus, a mutant allele of Npr2 gene encoding a natriuretic peptide receptor B, revealed that slw locus is an allele of the Npr2 gene. These results suggest that the dwarf phenotype of the SLW mouse is caused by the disturbed endochondral ossification, and a mutation in the Npr2 gene is expected to be responsible for the phenotypes of the SLW mouse.

Corresponding Editor: Roger Reeves

Received November 18, 2006
Accepted June 26, 2007


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