It has been proposed that disruption of the microtubule (MT) cytoskeleton can contribute to heart disease. Dees et al. now provide genetic evidence to support this hypothesis by characterising mice with cardiomyocyte-specific knockout of CENP-F, a multifunctional MT-binding protein whose decreased expression was recently linked to end-stage dilated cardiomyopathy in humans. Mutant mice have smaller hearts with multiple defects including thinner ventricular walls, reduced myocyte proliferation and fewer intercalated discs (myocyte-specific junctional complexes responsible for electrical and force transduction). Mutant mice also develop progressive dilated cardiomyopathy, arrhythmias and cardiac fibrosis. These results reveal a new disease mechanism and suggest that mutations in other MT-associated proteins could also contribute to heart disease. Page 468

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