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Vol. 12, Issue 5, 1529-1539, May 2001

A Tropomyosin-2 Mutation Suppresses a Troponin I Myopathy in Drosophila

Benyoussef Naimi,* Andrew Harrison,* Mark Cummins,* Upendra Nongthomba,* Samantha Clark,* Inmaculada Canal,dagger Alberto Ferrus,dagger and John C. Sparrow*Dagger

 *Department of Biology, University of York, York YO10 5YW, United Kingdom; and  dagger Instituto Cajal, Consejo Superior de Investigaciones Científicas, Madrid 28002, Spain.

A suppressor mutation, D53, of the held-up2 allele of the Drosophila melanogaster Troponin I (wupA) gene is described. D53, a missense mutation, S185F, of the tropomyosin-2, Tm2, gene fully suppresses all the phenotypic effects of held-up2, including the destructive hypercontraction of the indirect flight muscles (IFMs), a lack of jumping, the progressive myopathy of the walking muscles, and reductions in larval crawling and feeding behavior. The suppressor restores normal function of the IFMs, but flight ability decreases with age and correlates with an unusual, progressive structural collapse of the myofibrillar lattice starting at the center. The S185F substitution in Tm2 is close to a troponin T binding site on tropomyosin. Models to explain suppression by D53, derived from current knowledge of the vertebrate troponin-tropomyosin complex structure and functions, are discussed. The effects of S185F are compared with those of two mutations in residues 175 and 180 of human alpha -tropomyosin 1 which cause familial hypertrophic cardiomyopathy (HCM).

Dagger Corresponding author. E-mail address: jcs1{at}york.ac.uk.

Molecular Biology of the Cell
Vol. 12, 1529-1539, May 2001
Copyright © 2001 by The American Society for Cell Biology


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