The Act88F promoter drives expression of a 1.14kb KpnI-PstI genomic fragment containing fln.

fln^Act88F.PB partially rescues fln⁰

fln^Act88F.PB significantly improves the flight performance of fln⁰ animals. The indirect flight muscle defects of fln⁰ animals are also largely rescued by fln^Act88F.PB. Sarcomeres appear normal in longitudinal sections, with well-defined Z-bands and clearly depicted A-bands and I-bands and sarcomere length is uniform and similar to that seen in wild-type flies. In cross-section, the rescued myofibrils are circular with a well defined diameter and show the normal double hexagonal array of interdigitated thick filaments and thin filaments. However, there are a decreased number of thick filaments per myofibril in the rescued animals. In addition, broken down sarcomeres with partially torn Z-bands and missing M-lines are occasionally seen, as well as myofibrils with fractures that suggest a faultily assembled lattice. The active viscoelastic properties of indirect flight muscle skinned fibres analysed by sinusoidal analysis are not significantly different in fibres isolated from rescued or control flies. Flight parameters of the rescued flies at maximum locomotor capacity (assayed in a virtual reality flight simulator) are slightly compromised compared to controls; the rescued flies generate enough flight force to sustain hovering flight but show reduced capability to produce forces in excess of hovering flight force. The rescued flies show a significant reduction in stroke frequency during flight compared to controls.