Addtive ultrastructural phenotypes of <i>snpn-1</i> and <i>snt-1</i> mutants suggest independent roles in the vesicle cycle.

<p>(A) Representative micrographs of neuromuscular junctions (NMJs) from 40 nm sections of specimens prepared by high-pressure freeze fixation (HPS). The neuronal presynaptic density in each synaptic profile is labeled PD, examples of docked synaptic vesicles (SV) are indicated with an arrowhead and cisternae are indicated by an arrow. The plotted data show that the mean ± SEM value for the number of synaptic vesicles per synaptic profile is reduced in <i>snt-1</i> but not <i>snpn-1</i> mutants (B) and that <i>snt-1</i>, but not <i>snpn-1</i> mutants exhibit significant increases in the number of cisternae, effects that are apparent in both <i>snt-1</i> single and <i>snt-1;snpn-1</i> double mutants. (C). Both <i>snt-1</i> mutant phenotypes are indicative of an endocytic defect. Plots of the number of SVs docked at the plasma membrane show reductions in both <i>snpn-1</i> and <i>snt-1</i> mutants, which are additive in the <i>snt-1;snpn-1</i> double (D), however, when the docking defect is plotted as a ratio of SVs in each profile, the docking defect only persists in the presence of the <i>snpn-1</i> mutant (E). Scale bar 200 nm.