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A more recent version of this article appeared on May 12, 2006
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M509561200v1
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Papers In Press, published online ahead of print March 10, 2006
J. Biol. Chem, 10.1074/jbc.M509561200
Submitted on August 30, 2005
Revised on March 7, 2006
Accepted on March 10, 2006

Increased Ca2+-affinity of cardiac thin filaments reconstituted with cardiomyopathy-related mutant cardiac troponin I

Tomoyoshi Kobayashi and R . John Solaro

Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL 60612

Corresponding Author: tkoba{at}uic.edu

In order to understand the molecular mechanisms whereby cardiomyopathy-related cardiac troponin I (cTnI) mutations affect myofilament activity, we have investigated the Ca2+-binding properties of various assemblies of the regulatory components that contain one of the cardiomyopahty-related mutant cTnI. Acto-S1 ATPase activities in reconstituted systems were also determined. We investigated R145G and R145W mutations from the inhibitory region and D190H and R192H mutations from the second actin-tropomyosin binding site. Each of the four mutations sensitized the acto-S1 ATPase to Ca2+. Whereas the mutations from the inhibitory region increased the basal level of ATPase activity, those from the second actin-tropomyosin binding site did not. The effects on the Ca2+-binding properties of the troponin ternary complex and the troponin-tropomyosin complex with one of four mutations were either desensitization or no effect compared with those with wild-type cTnI. All of mutations, however, affected the Ca2+-sensitivities of the reconstituted thin filaments in the same direction as the acto-S1 ATPase activity. Also the thin filaments with one of the mutant cTnIs bound Ca2+ with less cooperativity compared with those with wild-type cTnI. These data indicate that the mutations found in the inhibitory region and those from the second actin-Tm site shift the equilibrium of the states of the thin filaments differently. Moreover, the increased Ca2+ bound to myofilaments containing the mutant cTnIs may be an important factor in triggered arrhythmias associated with the cardiomyopathy.


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