Mutant wandering stage third instar larvae show heart defects compared to controls; they have a decreased shortening fraction, indicating reduced cardiac contractility. The same fraction of mutant and wild-type larvae show chamber shortening contractions, but there is a noticeable increase in the frequency at which these contractions occur in the mutant larvae. Arrhythmia is increased in the mutant hearts compared to controls. The velocity of movement of the heart chamber wall is decreased by 31% in mutant larvae compared to controls.
Homozygous border cell clones show normal migration.
Homozygous or heterozygous Tm23 mutants exhibit heart rates that are similar to wild-type flies but possess enlarged cardiac chambers and exhibit significant defects in systolic function and fractional shortening compared to controls.
Heterozygotes are able to jump short distances but are incapable of sustained flight.
Flight muscles of Tm23 are trapped in a relaxed state and cannot generate active force; tight-binding rigor cross-bridges can, however, form. In the absence of ATP the muscle fibers have a high stiffness and force.
Heterozygotes have poor flight ability and a normal wing posture. Homozygotes are flightless and have a normal wing posture.
Flightless mutant, having structurally and functionally abnormal flight muscles. Myofibrils are structurally much weaker than wild type, broken myofibril ends are frayed. In peripheral regions of myofibrils thick and thin filaments are poorly organised.
identical to Tm25
Tm23/Tm2[+] is an enhancer of indirect flight muscle cell phenotype of DAAMEx1