Muscle LIM protein (MLP) can be found at the Z-disk of sarcomeres where it is 
hypothesized to be involved in sensing muscle stretch. Loss of murine MLP 
results in dilated cardiomyopathy, and mutations in human MLP lead to cardiac 
hypertrophy, indicating a critical role for MLP in maintaining normal cardiac 
function. Loss of MLP in Drosophila (mlp84B) also leads to muscle dysfunction, 
providing a model system to examine MLP's mechanism of action. Mlp84B-null flies 
that survive to adulthood are not able to fly or beat their wings. Transgenic 
expression of the mlp84B gene in the Mlp84B-null background rescues flight 
ability and restores wing beating ability. Mechanical analysis of skinned flight 
muscle fibers showed a 30% decrease in oscillatory power production and a slight 
increase in the frequency at which maximum power is generated for fibers lacking 
Mlp84B compared with rescued fibers. Mlp84B-null muscle fibers displayed a 25% 
decrease in passive, active, and rigor stiffness compared with rescued fibers, 
but no significant decrease in isometric tension generation was observed. Muscle 
ultrastructure of Mlp84B-null muscle fibers is grossly normal; however, the null 
fibers have a slight decrease, 11%, in thick filament number per unit 
cross-sectional area. Our data indicate that MLP contributes to muscle stiffness 
and is necessary for maximum work and power generation.