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).
