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.