Key result
Addition of caldesmon fragment 606C shifted tropomyosin to the inner domain of actin, away from strong myosin binding sites, indicating a different structural mechanism from troponin.
Caldesmon and troponin act by different structural mechanisms to modulate muscle filament activity.
Distinguishes caldesmon from troponin via tropomyosin positioning in reconstituted filaments; leaves open relevance to intact smooth muscle or cardiovascular regulation.
Caldesmon inhibits actomyosin ATPase and filament sliding in vitro, and therefore may play a role in modulating smooth and non-muscle motile activities. A bacterially expressed caldesmon fragment, 606C, which consists of the C-terminal 150 amino acids of the intact molecule, possesses the same inhibitory properties as full-length caldesmon and was used in our structural studies to examine caldesmon function. Three-dimensional image reconstruction was carried out from electron micrographs of negatively stained, reconstituted thin filaments consisting of actin and smooth muscle tropomyosin both with and without added 606C. Helically arranged actin monomers and tropomyosin strands were observed in both cases. In the absence of 606C, tropomyosin adopted a position on the inner edge of the outer domain of actin monomers, with an apparent connection to sub-domain 1 of actin. In 606C-containing filaments that inhibited acto-HMM ATPase activity, tropomyosin was found in a different position, in association with the inner domain of actin, away from the majority of strong myosin binding sites. The effect of caldesmon on tropomyosin position therefore differs from that of troponin on skeletal muscle filaments, implying that caldesmon and troponin act by different structural mechanisms.
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Hodgkinson et al. (1997) studied this question. caldesmon fragment 606C vs. without added 606C was evaluated on tropomyosin position on actin monomers. Addition of caldesmon fragment 606C shifted tropomyosin to the inner domain of actin, away from strong myosin binding sites, indicating a different structural mechanism from troponin.
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