Abstract
The aperC (abnormal proboscis extension reflex C) mutation in Drosophila melanogaster causes a defect in the proboscis extension reflex (PER) in aged flies. Young flies of the mutant show an apparently normal PER. When aperCTF36 mutants were reared at 25 degrees C, the flies became unable to extend the proboscis at Day 5 of eclosion, but within a few days, many of them recovered the PER. When reared at 18 degrees C, the mutants showed a defective PER, but did not show the recovery. At 29 degrees C, only a limited number of the mutant flies showed the defective PER. Histological inspection of the mutant revealed that the degeneration occurs in a pair of muscles, the rostral protractors, which are involved in the extension of the rostrum. The degeneration of the muscle was observed in the mutant by polarizing light microscopy. The cross striation disappeared from the central portion of the muscle fibers at Day 3. Birefringence of the fibers also disappeared. At Day 10 the degenerated muscle fibers showed regeneration. The PER was closely correlated with the degree of muscle degeneration and regeneration. Temperature-shift experiments indicated that the temperature-sensitive-period of the aper CTF36 mutation occurs around Days 2-4 after eclosion. Results indicate that the aperC+ gene regulates the posteclosional maintenance of the muscle fibers.
