A Drosophila melanogaster model of diastolic dysfunction and cardiomyopathy based on impaired troponin-T function.

ABSTRACT:

Rationale

Regulation of striated muscle contraction is achieved by Ca2+ -dependent steric modulation of myosin cross-bridge cycling on actin by the thin filament troponin-tropomyosin complex. Alterations in the complex can induce contractile dysregulation and disease. For example, mutations between or near residues 112 to 136 of cardiac troponin-T, the crucial TnT1 (N-terminal domain of troponin-T)-tropomyosin-binding region, cause cardiomyopathy. The Drosophila upheld(101) Glu/Lys amino acid substitution lies C-terminally adjacent to this phylogenetically conserved sequence.

Objective

Using a highly integrative approach, we sought to determine the molecular trigger of upheld(101) myofibrillar degeneration, to evaluate contractile performance in the mutant cardiomyocytes, an

SUBMITTER: Viswanathan MC 

PROVIDER: S-EPMC4526186 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature