photoreceptor cell & axon
Illumination of dissociated, patch-clamped ommatidia from trp9;trpl302 double mutants show activation of the whole phototransduction cascade, do not show any light-induced current or Ca[2+] influx, but do show a normal light-dependent modulation of the delayed rectifier current mediated by Shab channels. Increasing the light level by a factor of ten results in an upregulation of approximately 30% and recovery to baseline within 30 minutes, similar to wildtype controls.
presynaptic terminal independently of cartridge composition. The photoreceptor terminals of these mutants show an increase in glial invaginations.
trp9 ; trpl302 double mutants show a reduced depolarisation response to anoxia in the photoreceptors compared to wild-type flies; the amplitude of anoxia-induced depolarisation in the double mutants is half that of wild type and the response kinetics are much slower than normal.
In trp9,trpl302 double mutants the second, large phase depolarization response to anoxia (caused by N2 and measured in the eye by extracellular voltage change recordings), fails, indicating that the small but not the large phase of the response resulted from accumulation of K+ in the extracellular space. In trp9, trpl302 double mutants the Ca2+ response to anoxia is virtually abolished.
Rhabdomeres of trpl302,inaD1 double mutants are intact in 1 day old flies. ERG light responses of trpl302,inaD1 and trpl302,trp2 are small and transient, but the response amplitude of trpl302,inaD1 is significantly smaller than that of trpl302,trp2. Similarly, refractory period and response latency defects are more severe for trpl302,inaD1 than for trpl302,trp2.
Double mutant analysis comparing the receptor potentials of trpl302 with inaFP106x; trpl302 or trp2; trpl302 or trp9; trpl302 showed that the effects of inaFP106x are as severe as those of trp2 and are specific to the trp channel.
Whole-cell patch-clamp recordings of photoreceptors display sensitivity and response kinetics indistinguishable from wild type. trpl302; trp2 mutants display a dramatic loss of responsiveness, the residual current is due to a small amount of functional trp channel. trpl302; trp2 mutants exhibit a dramatic bump phenotype.
The presence of trp::trplninaE.trp1-675.trpl681-1124.T:Avic\GFP-EGFP in trpl302; trp9 double mutants results in a response to light that declines towards baseline during prolonged intense light.
The presence of trp::trplninaE.trpl1-336.trp328-675.trpl681-1124.T:Avic\GFP-EGFP in trpl302; trp9 double mutants results in a response to light that declines towards baseline during prolonged intense light.
The presence of trp::trplninaE.trp1-328.trpl336-681.trp675-1275.T:Avic\GFP-EGFP in trpl302; trp9 double mutants results in a response to light that declines towards baseline during prolonged intense light.
Expression of trplScer\UAS.cZa under the control of either Scer\GAL4Gr66a.PD or Scer\GAL4trpl.PZ restores normal camphor avoidance and camphor-induced action potentials in S6 sensilla in trpl302 flies.