(Alliance, FBgn0016975 )

Adapter protein involved in endocytic recycling of synaptic vesicles membranes. May act by mediating the retrieval of synaptotagmin protein Syt from the plasma membrane, thereby facilitating the internalization of multiple synaptic vesicles from the plasma membrane.

(UniProt, Q24212)

Exists as temperature-sensitive behavioral, temperature-sensitive lethal, and unconditionally lethal alleles. Severe behavioral debilitation is quickly induced by shift of adult stn6 and stn7 from 25 to 29; abnormalities at high temperature include uncoordinated leg and wing movements, with complete paralysis never occurring (e.g., legs still move); stn6 causes some debilitation at 22 (slow movements, occasionally falling over); whereas stn7 is more nearly normal at low temperatures, and can even walk with difficulty at 29; at permissive temperatures, stn (allele unspecified) causes unusual jump response to light-off stimulus, which is more pronounced in combination with w (Kelly, 1983b); associated with this abnormal jumping is an increase in amplitude of light-off transient spike of electroretinogram (ERG); in tests of light-adapted mutant, the jump response, as monitored by recordings from indirect flight muscles, habituates with increasing frequencies of light-off stimulation (Kelly, 1983b); combining stn with tan, which by itself leads to decreased amplitude of ERG on and off transients, leads to loss of anomalous jumping and partial restoration of light-off spike. In biochemical experiments, stn (allele unspecified) found to cause accentuation of in vivo phosphorylation of a protein from adult head synaptosomal fractions that is modified in this way by a cAMP-dependent protein kinase, with such phosphorylation being enhanced by exposure of flies to light, prior to extraction (Kelly, 1983a). A protein, which has same molecular weight as the one noted above, found to be phosphorylated in vitro by a fly-derived Ca2+-calmodulin-dependent protein kinase; stn causes increased levels of in vivo phosphorylation of this material (Kelly, 1983b). The temperature-sensitive lethal allele, stn, leads to brief paralysis, followed by sporadic movements, as a result of mechanical shocking (Homyk and Sheppard, 1977, Genetics 87: 95-104); other abnormalities include abnormally short jump and flight distances, apparent absence of on and off transients in ERG, and lethality when raised at 29. Effects of three of the lethal alleles, stn1, stn11, and stn14, were examined during development for effects on gross anatomy of CNS or PNS; no obvious abnormalities were observed (Perrimon et al., 1989).