Essential light chains are required for full isometric force production by skeletal muscle myosin, likely due to altered crossbridge kinetics.
ELC but not RLC is essential for skeletal myosin force in vitro; hypothesis-generating for light-chain roles in human muscle disorders.
Myosin, a molecular motor that is responsible for muscle contraction, is composed of two heavy chains each with two light chains. The crystal structure of subfragment 1 indicates that both the regulatory light chains (RLCs) and the essential light chains (ELCs) stabilize an extended alpha-helical segment of the heavy chain. It has recently been shown in a motility assay that removal of either light chain markedly reduces actin filament sliding velocity without a significant loss in actin-activated ATPase activity. Here we demonstrate by single actin filament force measurements that RLC removal has little effect on isometric force, whereas ELC removal reduces isometric force by over 50%. These data are interpreted with a simple mechanical model where subfragment 1 behaves as a torque motor whose leyer arm length is sensitive to light-chain removal. Although the effect of removing RLCs fits within the confines of this model, altered crossbridge kinetics, as reflected in a reduced unloaded duty cycle, probably contributes to the reduced velocity and force production of ELC-deficient myosins.
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VanBuren et al. (1994) studied this question.
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