The neuromuscular junctions (NMJs) in Timp^S1 mutant third instar larvae have expanded arbors occupying a larger muscle surface area with increased number of boutons compared to controls.

Timp^S1 mutant NMJs show defects in synaptic vesicle 'loading' (measure of endocytosis) assayed by depolarization-dependent incorporation of the FM1-43 lipophilic dye. The loading of the dye in Timp^S1 mutant NMJs is decreased overall compared to wild-type controls and is also much more variable across individual boutons. The level of residual dye after its depolarization-dependent release, 'unloading' (measure of exocytosis), is similar to controls but if normalized for the reduced initial loading, then the percentage of the dye released is decreased in the mutants.

Timp^S1 mutant larvae display locomotion defects: the individual peristaltic waves that propel the larvae forwards are significantly slower and the contraction wave pattern is less uniform and more variable than in controls, although there is a trend toward reduced velocity relative to wild-type controls, the difference is not statistically significant. However,the Timp^S1 larvae display a significant decrease in exploratory turning behavior. This peristalsis defects are also observed in Df(3R)Timp-Syn²⁸ (a deficiency spanning both Timp and Syn genes) mutants but not in Syn⁹⁷ larvae suggesting the phenotype is indeed due to perturbation of the Timp gene.

Timp^S1 (as well as Df(3R)Timp-Syn²⁸) mutant adults have reduced survival rate and also show wing defects (misshapen wings with blisters and necrotic patches).

Timp^S1 has abnormal locomotor behavior | third instar larval stage phenotype, suppressible by gbb²/gbb[+]

Timp^S1 has NMJ bouton | increased number | third instar larval stage phenotype, suppressible | partially by gbb²/gbb[+]