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Genetics, Vol. 164, 209-222, May 2003, Copyright © 2003

Suppression of Muscle Hypercontraction by Mutations in the Myosin Heavy Chain Gene of Drosophila melanogaster

Upendra Nongthombaa, Mark Cumminsa, Samantha Clarka, Jim O. Vigoreauxb, and John C. Sparrowa
a Department of Biology, University of York, York YO10 5YW, United Kingdom
b Department of Biology, University of Vermont, Burlington, Vermont 05405-0086

Corresponding author: John C. Sparrow, University of York, York YO10 5YW, United Kingdom., jcs1{at}york.ac.uk (E-mail)

Communicating editor: T. SCHÜPBACH

The indirect flight muscles (IFM) of Drosophila melanogaster provide a good genetic system with which to investigate muscle function. Flight muscle contraction is regulated by both stretch and Ca2+-induced thin filament (actin + tropomyosin + troponin complex) activation. Some mutants in troponin-I (TnI) and troponin-T (TnT) genes cause a "hypercontraction" muscle phenotype, suggesting that this condition arises from defects in Ca2+ regulation and actomyosin-generated tension. We have tested the hypothesis that missense mutations of the myosin heavy chain gene, Mhc, which suppress the hypercontraction of the TnI mutant held-up2 (hdp2), do so by reducing actomyosin force production. Here we show that a "headless" Mhc transgenic fly construct that reduces the myosin head concentration in the muscle thick filaments acts as a dose-dependent suppressor of hypercontracting alleles of TnI, TnT, Mhc, and flightin genes. The data suggest that most, if not all, mutants causing hypercontraction require actomyosin-produced forces to do so. Whether all Mhc suppressors act simply by reducing the force production of the thick filament is discussed with respect to current models of myosin function and thin filament activation by the binding of calcium to the troponin complex.




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