Key result
The A400V mutation rendered full-length wild-type myosin almost completely inactive, while the reverse V400A mutation in the cardiac CM-loop chimera restored almost full activity.
Mutations in the cardiomyopathy loop of myosin II, including those analogous to human hypertrophic cardiomyopathy mutations, significantly alter biochemical kinetics and biological function in a Dictyostelium model.
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Dictyostelium model data on CM-loop mutations; hypothesis-generating for HCM mechanisms, should not yet change practice.
Liu et al. (2005) studied Familial hypertrophic cardiomyopathy (contextual). Mutations of the Cardiomyopathy Loop of Dictyostelium Myosin II vs. Wild-type myosin was evaluated on Biological functions (growth, capping, development) and biochemical activities (actin-activated MgATPase, in vitro motility). The A400V mutation rendered full-length wild-type myosin almost completely inactive, while the reverse V400A mutation in the cardiac CM-loop chimera restored almost full activity.
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