| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
CELLULAR |
1 Department of Bioengineering, University of Washington, Seattle WA 98195 USA
2
Department of Biological Science and Program in Molecular Biophysics, and Department of Chemical and Biomedical Engineering, Florida State University, Tallahassee, FL 32306-4370, USA
Thin-filament regulation of isometric force redevelopment (ktr) was examined in rabbit psoas fibres by substituting native TnC with either cardiac TnC (cTnC), a site I-inactive skeletal TnC mutant (xsTnC), or mixtures of native purified skeletal TnC (sTnC) and a site I- and II-inactive skeletal TnC mutant (xxsTnC). Reconstituted maximal Ca2+-activated force (rFmax) decreased as the fraction of sTnC in sTnC: xxsTnC mixtures was reduced, but maximal ktr was unaffected until rFmax was <0.2 of pre-extracted Fmax. In contrast, reconstitution with cTnC or xsTnC reduced maximal ktr to 0.48 and 0.44 of control (P < 0.01), respectively, with corresponding rFmax of 0.68 ± 0.03 and 0.25 ± 0.02 Fmax. The ktr–pCa relation of fibres containing sTnC: xxsTnC mixtures (rFmax > 0.2 Fmax) was little effected, though ktr was slightly elevated at low Ca2+ activation. The magnitude of the Ca2+-dependent increase in ktr was greatly reduced following cTnC or xsTnC reconstitution because ktr at low levels of Ca2+ was elevated and maximal ktr was reduced. Solution Ca2+ dissociation rates (koff) from whole Tn complexes containing sTnC (26 ± 0.1 s–1), cTnC (38 ± 0.9 s–1) and xsTnC (50 ± 1.2 s–1) correlated with ktr at low Ca2+ levels and were inversely related to rFmax. At low Ca2+ activation, ktr was similarly elevated in cTnC-reconstituted fibres with ATP or when cross-bridge cycling rate was increased with 2-deoxy-ATP. Our results and model simulations indicate little or no requirement for cooperative interactions between thin-filament regulatory units in modulating ktr at any [Ca2+] and suggest Ca2+ activation properties of individual troponin complexes may influence the apparent rate constant of cross-bridge detachment.
(Received 1 November 2006;
accepted after revision 18 December 2006;
first published online 4 January 2007)
Corresponding author M. Regnier: University of Washington, Department of Bioengineering, Box 357962, Seattle, WA 98195-7962, USA. Email: mregnier{at}u.washington.edu
This article has been cited by other articles:
|
|
 |
|
  K. L. Kreutziger, N. Piroddi, B. Scellini, C. Tesi, C. Poggesi, and M. Regnier Thin filament Ca2+ binding properties and regulatory unit interactions alter kinetics of tension development and relaxation in rabbit skeletal muscle J. Physiol., August 1, 2008; 586(15): 3683 - 3700. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. E. Gillis, C. R. Marshall, and G. F. Tibbits Functional and evolutionary relationships of troponin C Physiol Genomics, December 19, 2007; 32(1): 16 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Norman, J. A. Rall, S. B. Tikunova, and J. P. Davis Modulation of the rate of cardiac muscle contraction by troponin C constructs with various calcium binding affinities Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2580 - H2587. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. L. Kreutziger, T. E. Gillis, J. P. Davis, S. B. Tikunova, and M. Regnier Influence of enhanced troponin C Ca2+-binding affinity on cooperative thin filament activation in rabbit skeletal muscle J. Physiol., August 15, 2007; 583(1): 337 - 350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. B. Chase Tropomyosin in the groove? Molecular insights into an inherited myopathy J. Physiol., June 15, 2007; 581(3): 889 - 889. [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Martyn, L. Smith, K. L. Kreutziger, S. Xu, L. C. Yu, and M. Regnier The Effects of Force Inhibition by Sodium Vanadate on Cross-Bridge Binding, Force Redevelopment, and Ca2+ Activation in Cardiac Muscle Biophys. J., June 15, 2007; 92(12): 4379 - 4390. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
