PubMed1985
The mutation raised (rsd, 3-95.4) of Drosophila melanogaster causes flightlessness as a consequence of abnormalities in the fibrillar flight muscles (FFMs). In this muscle type actin III is neither synthesized nor accumulated while adult tubular muscles of rsd flies are indistinguishable from wildtype. This paper demonstrates ultrastructural defects in rds FFMs and extends the biochemical comparison of adult wildtype and rsd muscles to larval muscles and to embryo cells differentiating in culture. The FFMs of mature rsd flies contain thick filaments in irregular bundles, but no thin filaments. Normal Z-discs are virtually absent. Instead, a large number of Z-disc residues are present in stacks attached to short filaments on either side. In newly emerged rsd flies the disorganization is less pronounced. The adult tubular muscles and the supercontracting muscles of third-instar larvae of rsd can ultrastructurally not be distinguished from wildtype. The present biochemical results indicate that not only FFMs of mature and newly emerged adults are affected by the rsd genotype. Synthesis of actin III is not detectable in rsd FFMs which corresponds to the heavy structural defects. In addition to the lack of actin III synthesis in rsd FFMs, three unidentified proteins (52 kDa, 80 kDa, 90 kDa) which are specific for wildtype FFMs are also not synthesized in rsd flies. Among all other muscle types studied, all of which are morphologically unaffected, only adult tubular muscle of rsd genotype showed no biochemical effect. Larval supercontracting muscle as well as embryo cells differentiating in culture failed to synthesize actin III in the case of rsd cells.(ABSTRACT TRUNCATED AT 250 WORDS)