Nature Genetics 15,[131][132][133][134][135][136].Editorial changes after the authors correction of the proofs resulted in the incorrect substitution of the word 'eutherian' for the word 'therian' throughout the text. We would like to clarify that the lnfraclass Eutheria refers to the 'placental' mammals only, whereas the Subclass Theria includes both the Infraclass Metatheria (marsupials) and the Infraclass Eutheria. Substitutions of'therian' for 'eutherian' should be made on: page 131, Abstract, line 7; page 134, column 2, line 3; page 135, column I, paragraph 3, line 3; page 135, column 2, paragraph 3, line 14.These alterations substantially change the conclusions of the article, which are as follows: the presence of a single copy RBM gene in American and Australian marsupials suggests that RBM was originally present as a single copy on the Y chromosome of an ancestral therian mammal. Following the divergence of marsupials and eutherians approximately 130 million years ago, RBM has been amplified independently in several marsupial and eutherian lineages. The conserved testis-specific expression of RBM in both marsupials and eutherians suggests that the selection for a critical male-specific function ensured the retention of RBM on the mammalian Y chromosome.Nature Genetics regrets any confusion this might have caused.Promoter swapping between the genes for a novel zinc finger protein and ~-catenin in pleiomorphic adenomas with t(3;8)(p21 ;q 12) translocations Nature Genetics 15, 170-174 (1997).Two lines of the Pl.AG I sequence (nt 5300-5621) in the 3' untranslated region were inadvertently deleted from Fig. 2 a. The complete sequence for this region can be obtained from GenBank accession nwnber U65002. We apologize for any inconvenience created by this error.

Mutations in sarcomere protein genes account for approximately 10 percent of cases of familial dilated cardiomyopathy and are particularly prevalent in families with early-onset ventricular dilatation and dysfunction. Because distinct mutations in sarcomere proteins cause either dilated or hypertrophic cardiomyopathy, the effects of mutant sarcomere proteins on muscle mechanics must trigger two different series of events that remodel the heart.

No abstract

Familial hypertrophic cardiomyopathy is an autosomal dominant disorder manifesting as cardiac hypertrophy in the absence of increased cardiac work load, which has been studied as a model of myocardial hypertrophy in humans. Hypertrophic cardiomyopathy is genetically heterogeneous with three known disease-genes and two further mapped loci. The disease-genes encode contractile proteins of the thick and thin filaments of the sarcomere: the beta cardiac myosin heavy chain gene on chromosome 14q11, the alpha tropomyosin gene on chromosome 15q2 and the cardiac troponin T gene on chromosome 1q3. Other disease loci have been mapped to chromosome 11p13-q13 and 7q3. In each known disease-gene a number of different mutations have been identified; these are missense mutations, or mutations leading to modest alterations of peptide structure, but not null alleles. Specific mutations are associated with different disease severity and may provide diagnostic and prognostic information not available from clinical assessment. Genetic and functional data suggest that mutations which cause hypertrophic cardiomyopathy act as dominant negative alleles that impair cross-bridge cycling and contractile function and interfere with sarcomere assembly.