Specific Myosin Heavy Chain Mutations Suppress Troponin I Defects in Drosophila Muscles

Abstract. We show that specific mutations in the head of the thick filament molecule myosin heavy chain prevent a degenerative muscle syndrome resulting from the hdp 2 mutation in the thin filament protein troponin I. One mutation deletes eight residues from the actin binding loop of myosin, while a second affects a residue at the base of this loop. Two other mutations affect amino acids near the site of nucleotide entry and exit in the motor domain. We document the degree of phenotypic rescue each suppressor permits and show that other point mutations in myosin, as well as null mutations, fail to suppress the hdp 2 phenotype. We discuss mechanisms by which the hdp 2 phenotypes are suppressed and conclude that the specific residues we identified in myosin are important in regulating thick an