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Evaluation of candidate genes as a cause of chondrodysplasia in Labrador retrievers
Authors:Jelke Jan Smit  Jedee Temwitchitr  Bouvien AW Brocks  Peter GJ Nikkels  Herman AW Hazewinkel  Peter AJ Leegwater
Institution:1. Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, PO Box 80154, 3508 TD Utrecht, The Netherlands;2. Department of Pathology, Faculty of Medicine, University Medical Centre Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands;1. Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK;2. WildGenes Laboratory, Royal Zoological Society of Scotland, Edinburgh EH12 6TS, UK;3. Powell Torrance Diagnostic Services, Manor Farm Business Park, Higham Gobion, Hertfordshire SG5 3HR, UK;4. Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Onderstepoort 0110, South Africa;1. Institute of Farm Animal Genetics, Friedrich-Loeffler-Institut (FLI), Neustadt-Mariensee, Germany;2. Centre for Infectious Disease Control Netherlands (CIb), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands;1. Department of Dermatology, Peking University First Hospital, Beijing 100034, China;2. Beijing Key Laboratory of Molecular Diagnosis of Dermatoses, Beijing 100034, China;3. Department of Dermatology, University of North Carolina, Chapel Hill, NC, USA;1. Department of Veterinary Clinical Studies, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
Abstract:Chondrodysplasia (CD) is a disabling, hereditary disease in Labradors with short limbs, warranting genetic screening in families at risk. Segregation analysis of eight litters with 13 affected dogs showed that autosomal recessive inheritance was consistent with the observed incidence of CD in the litters. Possible involvement of eight candidate collagen genes (COL9A1, COL9A2, COL9A3, COMP, MATN3, COL2A1, COL11A1 and COL11A2) and of a sulfate transporter glycoprotein (SLC26A2) gene in eight affected dogs and in 14 related control Labradors was investigated. Assuming recessive inheritance, the candidate genes could not be implicated in CD.
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