UASt regulatory sequences drive expression of an inverted repeat.
Expression of VhaM8.9KK107676 driven by Scer\GAL4GMR.PF (together with UAS-dicer2 to enhance RNAi efficiency) does not lead to external eye morphology phenotypes, but flies show significant defects in phototaxis behavior compared to controls. Mutant ommatidia and photoreceptors show overall intact organization but photoreceptor-surrounding pigment cells are highly vacuolated and there is an accumulation of vesicular structures in photoreceptor cytoplasm. Electroretinograms (ERGs) from Scer\GAL4GMR.PF>VhaM8.9KK107676 eyes reveal synaptic defects, with complete absence of 'on' or 'off' transients and diminished amplitude photoreceptor re- and depolarization in response to light.
Expression of VhaM8.9KK107676 driven by Scer\GAL4elav.PLu (together with UAS-dicer2 to enhance RNAi efficiency) induces lethality at different development (primarily during larval stages) and surviving flies show reduced spontaneous movements and poor climbing ability. The area of synaptic terminals and number of active zones is significantly decreased and there is a significant increase in the number of satellite boutons at the neuromuscular junction in Scer\GAL4elav.PLu>VhaM8.9KK107676 third instar larvae, compared to controls; synapses also contain large multivesicular body-like organelles and T-bars at active zones are perturbed, and axonal transport defects are detected. Scer\GAL4elav.PLu>VhaM8.9KK107676 adult brains show impairments in autophagy.
Flies with expression of VhaM8.9KK107676 driven by Scer\GAL4247 show elevated activity in response to stimulation (such as banging or soft tapping), with repeated jumping, wing flapping and crashing. Male mutants show subtle defects in short-term (1hr) and complete absence of long-term (24hr) memory in a courtship conditioning paradigm (but show normal naive courtship levels).
ATP6AP2KK107676, Scer\GAL4hs.2sev is a suppressor | partially of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, fzUAS.cAa
ATP6AP2KK107676, Scer\GAL4hs.2sev is a suppressor | partially of ommatidium phenotype of Scer\GAL4hs.2sev, fzUAS.cAa
The planar polarity defects in the eye which are caused by expression of fzScer\UAS.cAa under the control of Scer\GAL4hs.2sev are partially suppressed by co-expression of VhaM8.9KK107676.