Mhc¹/+ adults show decreased end-diastolic diameter.

Dorsal longitudinal muscles of Mhc¹/+ individuals expressing Mhc^UAS.cDa under the control of Scer\GAL4^Mef2.PR show relatively normal muscle fibers and Z- discs, despite of a small frequency of fiber splitting. The pupal stage of these individuals takes longer than in controls. Adults show a mild reduction in climbing ability, as compared to controls.

Dorsal longitudinal muscles of Mhc¹/+ individuals expressing either Mhc^R672C.UAS, Mhc^R672H.UAS, or Mhc^T178I.UAS under the control of Scer\GAL4^Mef2.PR show progressive defects: severe fiber branching and splitting defects, smaller sarcomeres (shortening of the inter-Z disc distance and narrower Z discs) and fragmented Z discs (Kettin), compared to controls. The pupal stage of these individuals takes longer than in controls. Adults show a mild reduction in climbing ability, as compared to controls.

Mhc¹/Mhc¹ causes lethality.

Expression of Mhc^P838L/Mhc^P838L in a Mhc¹/Mhc¹ background results in no significant difference in heart myofibril arrangement and morphology, myofilament arrays, Z-disc and sarcomere morphology, heart period, diastolic diameter, systolic diameter or fractional shortening, as compared with controls. Expression of Mhc^P838L/+ in a Mhc¹/Mhc¹ background also does not result in any significant difference in sarcomere structure, heart period, diastolic diameter, systolic diameter or fractional shortening, as compared with controls (Mhc^+t12.4/Mhc^+t12.4 or Mhc^+t12.4/+ in a Mhc¹/Mhc¹ background).

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).

Homozygous clones in the dorsal air sac primordium are only rarely recovered.

Homozygous border cell clones show weak defects in migration.

The body wall muscles of Mhc¹ embryos show a more constant distance between thick and thin filaments than in wild type. However, the diameter of thick filaments is more variable than in wild-type muscle.

The gut muscles of Mhc¹ embryos show a higher degree of order than wild-type embryos.

Mhc¹ heterozygous flies are completely flightless.

The presynaptic terminals appear generally normal in homozygous embryos, although muscles are smaller and thinner than wild type. The properties of synaptic currents in longitudinal body-wall muscles in the mutant are similar to those in wild type.

Mhc¹ 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.

Embryos exhibit no muscular contractions and on examination no thick filaments are observed. Two copies of P{Mhc^emb} rescue the embryonic lethal Mhc¹ mutants to adults. Rescued adults do show phenotypic abnormalities: they are completely flightless, have reduced jumping ability, they can walk but are sluggish, often exhibit wings-up phenotype and have an indented thorax. Adults do not mate with each other but do with wild type. The myofibrils of Mhc¹; P{Mhc^emb} indirect flight muscles look normal. Myofibril stability is affected, a few days after eclosion fibrils are cracked and frayed, disruption is more extreme with time. Structure of the jump muscle is normal with only occasional minor deviations in the regularity of thick filament arrangement.

Myofibres of the indirect flight muscles of Mhc⁶/Mhc¹, Mhc¹³/Mhc¹ or Mhc¹⁹/Mhc¹ flies often appear bunched at one attachment site, although the myofibre surface does remain attached at both attachment sites.

Heterozygotes are flightless. Disruptions in the structure of the IFM myofibrils are seen - cracks are visible throughout the myofibril where no thick filaments are present.

Heterozygotes have normal wing posture, and normal running and climbing behaviours.

Homozygous embryos show no movement; unable to hatch; ultrastructural observations show complete lack of thick filaments in muscles. Heterozygotes display nearly a 50% reduction in the numbers of thick filaments in indirect flight muscles and the tergal-depressor-of-the-trochanter muscle, resulting in disruption of the normal regular array of thick and thin filaments in these muscles. Other less regularly organized muscles, although having reduced numbers of thick filaments, appear to function adequately in Mhc¹/+ flies (O'Donnell and Bernstein, 1988).