Homozygous Sesn8A11 mutants do not exhibit developmental abnormalities.
Fat bodies of homozygous Sesn8A11 mutant larvae contain more lipids than do those of wild-type animals.
The heart function of homozygous Sesn8A11 mutants is compromised, as manifested in arrhythmia and decreased heart rate. Sesn8A11 mutant hearts are dilated during both the diastolic and systolic phases. Myofibrils of Sesn8A11 mutant hearts display structural disorganisation.
20-day old Sesn8A11/Sesn3F6 mutant flies show degeneration of thoracic muscles with loss of sarcomeric structure, including discontinued Z discs, disappearance of M bands, scrambled actomyosin arrays, and diffused sarcomere boundaries. Such defects are only partially observed in very old wild-type flies (~90 days).
Despite its normal appearance, muscle from 5-day-old Sesn8A11/Sesn3F6 mutant flies exhibit mitochondrial abnormalities, including rounded shape, occasional enlargement, and disorganisation of cistae, which are also observed in 20-day old mutants.