Construct: Amino acid replacement: S18A.
Flies carrying the PrmS18A.cLa transgene exhibit significant defects in flight ability compared to wild-type. However, these flies do not exhibit defects in larval crawling speed. The indirect flight muscle myofibrils of these mutants are also assembled normally. There aren't any significant differences between control and mutant flies in major structural parameters such as sarcomere length, thick filament number per myofibril cross-sectional area, and percentage of myofibril area per muscle cross-sectional area. Mutant flies exhibit a 1.4-2.7% increase in myofibril cross-sectional area, although the number of thick filaments per fiber is unchanged. At peak Ca activation (pCa 5.0), over a wide range of oscillation frequencies, the magnitudes of the elastic modulus, viscous modulus, and power output from PrmS18A.cLa fibers were dramatically reduced compared to those of the control. The active elastic moduli of PrmS18A.cLa fibers is significantly less (values ranged from 23-37% at the frequencies assessed) than that of the control. The viscous moduli of active PrmS18A.cLa fibers are significantly less for most frequency values of >20Hz (values ranged from 21-59% less). Consequently, PrmS18A.cLa active fibers produce significantly less power compared with controls throughout most of the positive power-producing range (42% less at maximum power). In a relaxed condition (where no myosin crossbridges are strongly attached to actin), PrmS18A.cLa fibers exhibit a significant reduction in magnitude of elastic modulus between 2.5 and 40Hz (ranging from 25-37% less) compared with controls. In rigor conditions (no ATP, where myosin crossbridges are strongly attached), PrmS18A.cLa fibers exhibit dramatic reductions in elastic modulus (ranging from 40-49% less) over the entire frequency range and in viscous modulus (ranging from 28-51% less) at all frequencies except at 0.5 and 1000Hz. PrmS18A.cLa mutants do not exhibit any significant differences in active (pCa 5.0) muscle fiber kinetics.
PrmS18A.cLa rescues Prm1
The transgene PrmS18A.cLa rescues the embryonic lethal phenotype of Prm1 to adulthood.