Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations.

ABSTRACT: In cardiac muscle, the troponin (cTn) complex is a key regulator of myofilament calcium sensitivity because it serves as a molecular switch required for translating myocyte calcium fluxes into sarcomeric contraction and relaxation. Studies of several species suggest that ectotherm chordates have myofilaments with heightened calcium responsiveness. However, genetic polymorphisms in cTn that cause increased myofilament sensitivity to activating calcium in mammals result in cardiac disease including arrhythmias, diastolic dysfunction, and increased susceptibility to sudden cardiac death. We hypothesized that specific residue modifications in the regulatory arm of troponin I (TnI) were critical in mediating the observed decrease in myofilament calcium sensitivity within the mammalian taxa. We

SUBMITTER: Palpant NJ 

PROVIDER: S-EPMC3032286 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature