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Journal of Heredity Advance Access originally published online on November 12, 2007
Journal of Heredity 2008 99(1):73-80; doi:10.1093/jhered/esm090
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© The American Genetic Association. 2007. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Evaluation of 15 Candidate Genes for Dilated Cardiomyopathy in the Newfoundland Dog

Anje C. Wiersma, Polona Stabej, Peter A. J. Leegwater, Bernard A. Van Oost, William E. Ollier, and Joanna Dukes-McEwan

From the Small Animal Teaching Hospital, University of Liverpool, Leahurst, Chester High Road, Neston, CH64 7TE, United Kingdom (Wiersma and Dukes-McEwan); the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, 3508 TD Utrecht, The Netherlands (Wiersma, Stabej, and Leegwater); the Centre for Integrated Genomic Medical Research, Division of Epidemiology and Health Sciences, The University of Manchester, Manchester, M13 9PT, United Kingdom (Wiersma and Ollier); and the Department of Molecular Cell Biology, American University of the Caribbean, #1 University Drive at Jordan Road, Cupecoy, St Maarten, Dutch Antilles (van Oost)

Address correspondence to A. C. Wiersma at the address above, or e-mail: a.c.wiersma{at}uu.nl.

Dilated cardiomyopathy (DCM) is a disease of the myocardium, which causes heart failure and premature death. It has been described in humans and several domestic animals. In the Newfoundland dog, DCM is an autosomal dominant disease with late onset and reduced penetrance. We analyzed 15 candidate genes for their involvement in DCM in the Newfoundland dog. Polymorphic microsatellite markers and single Nucleotide Polymorphisms were genotyped in 4 families of Newfoundland dogs segregating dilated cardiomyopathy for the genes encoding {alpha}-cardiac actin (ACTC), caveolin (CAVI), cysteine-rich protein 3 (CSRP3), LIM-domain binding factor 3 (LDB3), desmin (DES), lamin A/C (LMNA), myosin heavy polypeptide 7 (MYH7), delta-sarcoglycan (SGCD), troponin I (TNNTI3), troponin T (TNNT2), alpha-tropomyosin (TPMI), titin (TTN) and vinculin (VCL). A Logarithm of the odds (LOD) score of less than –2.0 in 2-point linkage analysis indicated exclusion of all but 2 genes, encoding CSRP3 and DES. A (LOD) score between –1.5 and –2.0 for CSRP3 and DES makes these genes unlikely causes of DCM in this dog breed. For the phospholamban (PLN) and titin cap (TTN) genes, a direct mutation screening approach was used. DNA sequence analysis of all exons showed no evidence that these genes are involved in DCM in the Newfoundland dog.

Corresponding Editor: Ernest Bailey

Received February 22, 2007
Accepted September 25, 2007


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