Olson et al. (2001, pubmed:11273725) described 2 probands with familial dilated cardiomyopathy. One was a 27-year-old man whose father and paternal uncle died from heart failure at age 27 and 49 years, respectively. Because of suspected familial CMD, screening echocardiogram was performed when the proband was 17 years old but was reportedly normal. At 26 years of age, the proband developed shortness of breath, edema, and nonsustained ventricular tachycardia. He had no echocardiographic features of hypertrophic cardiomyopathy, coronary arteries were normal by angiography, and cardiac biopsy findings were nonspecific and consistent with idiopathic CMD. Despite aggressive medical therapy and implantation of an automatic cardioverter defibrillator, he died at age 27 while on a cardiac transplant waiting list. The second proband presented at 3 months of age with congestive heart failure and was diagnosed with idiopathic CMD based on echocardiographic findings; her heart failure progressed while on medical therapy and she underwent cardiac transplantation at 10 years of age. Electron microscopy of her explanted heart tissue revealed an abnormal sarcomere structure in which the thin filaments of many sarcomeres appeared irregular and fragmented; the sarcomeres were also contracted with decreased distance between Z bands and the sarcolemma had a scalloped appearance. The girl's mother, who had developed heart palpitations during pregnancy that recurred 6 months after delivery, was diagnosed with idiopathic CMD at 33 years of age based on echocardiographic and cardiac biopsy findings and the absence of coronary artery disease on angiography. She remained stable on minimal medical therapy. Family history included a maternal grandfather who had died at 59 years of age from presumed myocardial infarction, and his father and several sibs reportedly died in their 50s from heart disease. [From MIM:611878, 2016.02.02]

Dilated cardiomyopathy-1Y (CMD1Y) and left ventricular noncompaction-9 (LVNC9, MIM:611878) are caused by heterozygous mutation in the TPM1 gene. [From MIM:611878, 2016.02.02]

Tropomyosins are a family of actin-binding proteins encoded by 4 distinct genes. Each gene generates multiple striated muscle, smooth muscle, and cytoskeletal variants by alternative splicing, alternative promoter usage, and differential 3-prime end processing. Of the 4 human tropomyosin genes, TPM1 is the most versatile and encodes at least 10 tissue-specific variants via alternative splicing and/or the use of 2 promoters. The TPM1 variants encode proteins of either 248 or 284 amino acids (summary by Denz et al., 2004, pubmed:15249230). [From MIM:191010, 2016.02.02]

Many to many: 4 human to 2 Drosophila.