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. 56% of mutant adults have an upheld wing phenotype, 40% have their wings held down and 4% hold their wings in the normal position. 84% of the indirect flight muscle fibres of mutant adults are hypercontracted, 16% show a partial hypercontraction phenotype. 76% of Mhc¹⁰/Mhc¹³ adults have an upheld wing phenotype, 24% have their wings held down and 0% hold their wings in the normal position. 39% of the indirect flight muscle fibres of mutant adults are hypercontracted, 61% show a partial hypercontraction phenotype. 4% of Mhc^2B/Mhc¹³ adults have an upheld wing phenotype, 38% have their wings held down and 58% hold their wings in the normal position. 0% of the indirect flight muscle fibres of mutant adults are hypercontracted, 35% show a partial hypercontraction phenotype and 65% are normal.

Mhc¹³ interacts with Mhc^E1570K or Mhc^L1736P in trans to give muscle phenotypes that are intermediate between the two or show severe indirect flight muscle degeneration.

Myofibres of the indirect flight muscles of homozygous or Mhc¹³/Mhc¹ flies (but not of heterozygous flies) often appear bunched at one attachment site, although the myofibre surface does remain attached at both attachment sites. This phenotype develops as the fly ages, with the myofibres appearing normal immediately after eclosion. The myofibrils of the indirect flight muscles have ultrastructural abnormalities in adult flies; myofibrils appear "hyper-contracted" in some areas and pulled apart in others, sarcomeres are abnormal and the hexagonal packing of the thick and thin filaments is almost completely absent. The tergal depressor of the trochanter muscles have some defects; the thick and thin filaments are slightly less organised than normal and myofibrils are less rectangular in cross-section than normal.

A homozygous viable allele. The indirect flight muscles develop myofibrils with almost normal structures but within the first 12 hours of adult life these muscles 'super-contract' and the muscle mass moves to one or other muscle attachment site. The myofibrillar structure is destroyed and muscle proteolysis occurs.

Reduced viability when heterozygous with Df(2L)H20 or Mhc¹. Heterozygotes with Mhc¹ display a distinct alteration in the shape of the dorso-longitudinal muscles (DLM), the greater part of the muscle mass has 'contracted' toward the anterior thoracic attachment site.

Myofibres of the dorso lateral indirect flight muscles (DLMs) of heterozygotes with Mhc^- allele or homozygotes degenerate after adult eclosion. An extra copy of Mhc cannot rescue the mutant phenotype.

A dominant flightless mutation; in homozygotes but not heterozygotes, the myofibrils of dorsolateral indirect flight muscles, although displaying normal morphology at eclosion, degenerate with time so that each cell is composed of a narrow strip of material connected to a bulged-out region. Some areas of the cells contain over-contracted sarcomeres and others show arrays of thick and thin filaments splayed throughout the cytoplasm. Abnormal morphology is recessive. Unlike the situation with other Mhc mutations, the dominant flightlessness of Mhc¹³ not rescued by the addition of a second dose of Mhc⁺. homozygous viable