Abstract
The emergence of adult Drosophila melanogaster from the puparium is followed by the programmed degeneration of a number of muscle groups. We have isolated two X-linked mutants that delay the programmed death of at least some of these muscles. During eclosion, the fly makes use of a membranous sac, the ptilinum, which is later retracted into the head capsule. Six of the eight sets of muscles involved in the retraction then undergo degeneration. The muscle fibers initially show a gradual atrophy and then degenerate rapidly through fragmentation followed by absorption. In wild-type flies, this degeneration is obvious by 12 h after eclosion due to the loss of the birefringence of the muscles. Through mutagenesis with ethyl methanesulfonate, we isolated four mutants whose birefringence of the doomed muscles was retained even at 12 h. Mutants were genetically classified into two complementation groups; mcd-1 and mcd-2 (mcd: muscle cell death). The muscles of the mcd-1 mutants degenerate more slowly than that of the wild-type flies; the fibers enter the fragmentation step but are then not rapidly absorbed. In the mcd-2 mutants, the fibers atrophy more slowly than that in the wild-type flies and fail to undergo fragmentation. The difference in the process of the muscle death between the mcd-1 and the mcd-2 mutants suggests that at least two genes act on different steps in the process of muscle cell death.
