Expression of Mhc^P838L in a Mhc¹/Mhc⁵ background does not result in any significant difference in heart period or diastolic diameter, but does cause a significant increase in systolic diameter and decrease in fractional shortening, as compared with controls (Mhc^+t12.4 in a Mhc¹/Mhc⁵ background).

Mhc⁵/Mhc⁵ flies are flight defective. Myofibrils are similar to wild type in the indirect flight muscle in late pupae, but 2 days after eclosion there is severe disruption and disorganization of sarcomeric material, with myofibrillar destruction. Mhc⁵/Mhc⁵ heart tubes are more narrow than wild type and show perturbed diastolic function; by 5 weeks old, nearly all hearts show some sign of restriction and impaired diastolic function. 3 week old Mhc⁵/Mhc⁵ heart preparations show fairly regular contractions that progressively worsen with age. At every age, mutant hearts show decreases in systolic diameters and have compromised ejection abilities throughout life compared to controls; mutant hearts also show significant rate increases in SI compared to controls.

The jump muscle output of 4 day old Mhc⁵ flies (measured using displacement of an ergometer) is decreased compared to control flies, while in 1 day old flies there is no significant difference between the jump muscle output of Mhc⁵ and wild-type flies.

The TDT muscle contains thick and thin filaments, but no clearly defined myofibrils, in Mhc⁵ flies. The thick filaments are no longer in a parallel lattice. The mitochondria still retain recognisable cristae, but small clear areas are apparent at the centre of some of them.

55% of Mhc⁵/+ flies show mild indirect flight muscle defects, in which some muscles are missing or abnormally-shaped muscles and or the DLM (dorsal medial muscle) template is split. 30% of these mutants show severe defects in which most thoracic sections show missing or abnormally-shaped muscles.

Correlating with the behavioural defects, abnormal spiking activity in the dorsal longitudinal muscles is observed at restrictive temperatures (38^oC) in Mhc⁵/+ mutants.

Heterozygous adults have variable flight ability; 20% have an indented thorax and are flightless, the remainder have a normal thorax and can fly, although poorly. The flight behaviour of heterozygotes is not noticeably improved by two copies of Mhc⁺, suggesting this allele is an antimorph. Hemizygotes are flightless. Homozygotes have a upheld wings.

Rank: RK2 Heterozygotes and homozygotes usually have a large indentation on the dorsal thorax near the attachment of the head. Newly eclosed adults appear normal except for shallow ridges on the thorax, the deep indentations arise from the movements made during the first few minutes of adult life. The phenotype shows approximately 95% penetrance in heterozygotes and approaches 100% penetrance in homozygotes. The homozygous phenotype is generally more abnormal, but not easily distinguished from the heterozygous phenotype.

20% of heterozygotes display indented thorax and erect wings and are flightless; the remainder have normal phenotype but fly poorly. Homozygotes display erect wing phenotype. Judged to be antimorphic since not rescued by addition of Dp(2;3)osp³. Mhc⁵ interaction in double heterozygotes with other flightless mutants observed by Homyk and Emerson (1988). Heterozygous viability severely reduced in combination with hemizygous wupA^hdp-2, up^int-3, up¹⁰¹; or up^x; rare escapers have gnarled legs, walk poorly, and die within two days of eclosion. Females doubly heterozygous for Mhc⁵ and wupA^hdp-2, up^int-3, up¹⁰¹; or up^x have normal viability but are completely flightless and display abnormal wing posture. homozygous viable

Mhc⁵, wupA^hdp-2 has lethal phenotype

Mhc⁵, up^int-3 has visible | dominant phenotype

Mhc⁵, up^int-3 has flightless | dominant phenotype

Mhc⁵, wupA^hdp-2 has visible | dominant phenotype

Mhc⁵, wupA^hdp-2 has flightless | dominant phenotype

Mhc⁵, up¹⁰¹ has visible | dominant phenotype

Mhc⁵, up¹⁰¹ has flightless | dominant phenotype

Mhc⁵, up^x has visible | dominant phenotype

Mhc⁵, up^x has flightless | dominant phenotype