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.

Transgenic flies expressing fln^Act88F.PB in a homozygous fln⁰ mutant genetic background are flight capable.

Indirect flight muscle thick filaments from newly eclosed fln⁰ flies are more variable in length and, on average, are significantly longer than wild-type filaments from flies of the same age. In the absence of fln, thick filaments can attain lengths >300% of wild-type filaments, indicating that fln is required for setting the proper filament length. Filaments lacking fln are structurally compromised, and filament preparations from fully matured 3- to 5-day old adult fln⁰ indirect flight muscles yield fragments of variable length much shorter than those from wild-type flies of a similar age. Newly eclosed fln⁰ flies exhibit indirect flight muscle filaments with larger bend angles along their entire length, in comparison with wild-type flies, and do not show the general increase in rigidity from the center to the tips that is typical of wild-type filaments.

The thick and thin filaments of the indirect flight muscles of homozygous animals appear normal at eclosion. In flies more than 2 days old, the fibres show a hypercontraction phenotype. 16% of mutant adults have an upheld wing phenotype, 24% have their wings held down and 60% hold their wings in the normal position. 76% of the indirect flight muscle fibres of mutant adults are hypercontracted, 24% show a partial hypercontraction phenotype.

Homozygotes and fln⁰/Df(3L)fln1 hemizygotes are flightless and show defects in their wing position, holding their wings ventrolaterally as opposed to dorsally. The dorsolongitudinal muscle (DLM) of many late-stage pupae and pharate adults are wavy. Some fibres are narrower than normal and/or misoriented with respect to the anterior-posterior body axis. The two longest DLM fibres located nearer the ventral thorax appear more severely affected than the other four DLM fibres. Regions near the myotendon junction appear very disordered. The morphology of the DLM fibres changes dramatically during the first day of adult life from long and wavy to shortened and torn, so that only small remnants of the DLM fibres remain attached to the cuticle in 1 day old adults. Fibres in which the bulk of the mass appears to be pulled towards one of the cuticle anchoring sites, most often toward the anterior end, are often seen, resulting from rupture of the myotendon junction from the opposite end. The degeneration of the DLM fibres is complete by 8 hours after eclosion. The myofibrils in the DLM of late stage pupae only stay well oriented for two or three sarcomere lengths. The sarcomeres are narrower and longer than wild type, and the length varies over a wider range. The thick filaments are longer than normal, as are the thin filaments, which extend to the M line. Sarcomere assembly appears normal in pupal mutant indirect flight muscles (IFMs), although the myofibrils have fewer thick filaments across the myofibril diameter compared to wild type. Adult IFMs show a wide variation in sarcomere length, ranging from 1.4 to 3.3 μm (wild-type IFM sarcomere length is between 3.1 and 3.3 μm). Adult sarcomeres become severely disordered. Initially, a wave of degeneration is seen along the same myofibril, with disorder increasing towards one end, but as the fly ages the entire IFM degenerates. Defects seen include separation of the Z bands and filaments laterally into smaller bundles, gradual decrease of Z-band spacing, disappearance of the thick filaments (especially from the M band region) and thin filament "cowlicks" projecting out of the sarcomere or bowing out of the myofibril. Dense particles are seen associated with the myofibril (this distribution of particles is not seen in wild-type myofibrils).

The indirect flight muscle (IFM) fibres of mutant adults reach a severely shortened state by approximately 5 hours following eclosion. The sarcomeres and thick filaments of mutant pupal IFMs are 25-30% longer than wild type and muscle fibres are abnormally wavy. Sarcomere assembly and myotendon junction structure are otherwise normal in pupae. In one day old adults however, the IFMs are severely disrupted and variably shortened, and myofibrils are ruptured at the myotendon junction. Unusual empty pockets and granular material appear in the middle of many adult mutant sarcomeres.

fln⁰ has indirect flight muscle cell phenotype, suppressible by Mhc[+]/Mhc^2B

fln⁰ has wing phenotype, suppressible by Mhc[+]/Mhc^2B