Transgenic flies expressing fln^ΔC44.Act88F in a wild-type genetic background show normal behaviour and flight ability.

Transgenic flies carrying fln^ΔC44.Act88F in a homozygous fln⁰ mutant genetic background can not beat their wings. The mutants are unable to produce any sustained, consistent wing movement emulating wing beats, although sporadic, small-amplitude wing motions are observed. The mutant flies display disorganised sarcomeric structure and disordered myofilament lattice. Although the mutants show cylindrical myofibril cross sections and sarcomeres with well defined Z-lines, the filament lattice appear disordered and M-lines are often absent or show reduced intensity. In some mutant sarcomeres the M-line appear wavy or zigzagged with electron dense material streaming into the A-band overlap zone. Irregularities in Z-band structure are also observed. Another common feature of the mutant sarcomeres is gaps along the A-band which occasionally runs the length of the sarcomere. These longitudinal gaps may be consistent with separations of the lattice that appear in the cross-sectioned images, disrupting the nearly crystalline hexagonal lattice found in wild-type indirect flight muscles. The mutant muscles display a decrease in inter-thick filament spacing and an increase in heterogeneity among myofibrils. Muscle fibers from transgenic flies expressing fln^ΔC44.Act88F in a homozygous fln⁰ mutant genetic background show decreased cross-bridge cycling kinetics. The mutant fibers produce roughly one third the oscillatory and power of that of wild-type, with reduced frequencies of maximum work and power output relative to wild-type.