Calcium-binding protein involved in exocytosis of vesicles filled with neurotransmitters and neuropeptides. May specifically mediate the Ca(2+)-dependent exocytosis of large dense-core vesicles (DCVs) and other dense-core vesicles. However, it probably also participates in small clear synaptic vesicles (SVs) exocytosis and it is unclear whether its function is related to Ca(2+) triggering. Membrane-associated to vesicles. Restricted to all classes of presynaptic termini independent of the ratio of vesicular content (dense core vesicles versus synaptic vesicles). Found in all identified classes of peripheral and central synapses. In the CNS, it is highly enriched in the synapse-dense neuropil, which lacks cell bodies. Present in all synapses in the neuropil where it precisely colocalizes with other pansynaptic markers. Similarly abundant in all classes of neuromuscular junction (NMJ) termini, including type I, II, and III NMJs, where it localizes to all 3 bouton types. Expressed at similar levels in boutons which contain primarily small clear glutamatergic vesicles, as well as boutons very highly enriched in large DCVs. It appears that neither bouton class contains a pure population of either SVs or DCVs, but only differs dramatically in the relative abundance of the vesicular classes. Thus, the level of expression does not correlate with the abundance of DCVs. Clearly present presynaptically and colocalizes exclusively with presynaptic markers. Restricted to the nervous system at all stages of development and highly localized at synapses (at protein level). Not detected in early embryos through stage 8. Strongly expressed in neural-specific cells at the onset of early stages of neuronal differentiation beginning at stage 9-10. Accumulates from stage 12 through the rest of embryogenesis in all neuronal cells within the brain and ventral nerve cord (VNC). Remains restricted to the central nervous system and not detected in other tissues at any stage of development. The PH domain is essential for regulated exocytosis and binds phospholipids. Flies display locomotory deficits and complete embryonic lethality. The mutant NMJ reveals a 50% loss in evoked glutamatergic transmission, and an accumulation of synaptic vesicles at active zones. They also display a 3-fold accumulation of DCVs in synaptic terminals. Incomplete sequence. Truncated N-terminus.