G29137351A
G to A mutation in the splice acceptor site.
Nucleotide substitution: G?A.
Mutation of the splice acceptor site at the start of exon 10.
lethal (with Df(3R)3450)
Vha100-14 mutant photoreceptor clones display defects in neurotransmission, as shown by loss of "on" transients in electroretinogram (ERG) recordings.
The electroretinogram of mutant photoreceptors lacks the on transient.
Mutant photoreceptor neurons show a reduction in acidification (measured using Lysotracker fluorescence) at 40% of pupal development compared to wild-type cells. Acidification before neuronal differentiation is normal in the mutants.
Mutant photoreceptor terminals contain aberrant multivesicular structures and double-membrane autophagosomal vacuoles.
Animals expressing Vha100-1R755A.Scer\UAS under the control of Scer\GAL4unspecified in a Vha100-14 background show loss of photoreceptors and have a reduced eye phenotype.
The electroretinogram depolarisation is indistinguishable from wild type in 1 week old mutant photoreceptors. However, a weak reduction in depolarisation becomes apparent after 3 weeks and progressively worsens by 5 weeks. This progressive reduction in depolarisation is seen under both 12 hour light: 12 hour dark and constant darkness conditions. The 5 week old mutant photoreceptors show a loss of most discernible rhabdomere structure.
Flies in which the retina is homozygous for Vha100-14 (made using the 'ey-flp' system described in FBrf0125463) consistently fail to walk toward light in a phototaxis assay. Electro-retinograms from these animals display normal depolarization in response to light stimuli, but exhibit a complete loss of 'on' and 'off' transients, indicative of a failure to evoke a postsynaptic response.
Scer\GAL4GMR.PF, Scer\GAL4GMR.PF, Vha100-14 is a suppressor | partially | somatic clone of eye phenotype of Syx1AUAS.cBa/Syx1AScer\UAS.cBa
Scer\GAL4GMR.PF, Scer\GAL4GMR.PF, Vha100-14 is a suppressor | partially | somatic clone of ommatidium phenotype of Syx1AUAS.cBa/Syx1AScer\UAS.cBa
The rough eye phenotype of Syx1AScer\UAS.cBa; Scer\GAL4GMR.PF flies raised at 18oC is largely suppressed when the eye is made homozygous for Vha100-14.
Vha100-14 is rescued by Vha100-1N509Q.UAS/Scer\GAL4GMR.PF
Df(3R)3450/Vha100-14 is rescued by Scer\GAL4elav-C155/Vha100-1N509Q.UAS
Vha100-11/Vha100-14 is rescued by Vha100-1+tCH322-119J05
Vha100-14 is partially rescued by Scer\GAL4unspecified/Vha100-1R755A.UAS
Expression of Vha100-1N509Q.Scer\UAS under the control of Scer\GAL4GMR.PF fully rescues the neurotransmission defects seen when photoreceptors are mutant for Vha100-14.
Expression of Vha100-1N509Q.Scer\UAS under the control of Scer\GAL4elav-C155 fully rescues the lethality seen in Vha100-14/Df(3R)3450 mutants.
The on transient of the electroretinogram is significantly rescued in Vha100-14 mutant photoreceptors in which Vha100-1R755A.Scer\UAS is expressed under the control of Scer\GAL4unspecified, although this is accompanied by a pronounced decrease in electroretinogram depolarisation.
The acidification defects seen in Vha100-14 mutant photoreceptors after neuronal differentiation are not rescued by expression of Vha100-1R755A.Scer\UAS in the photoreceptors under the control of Scer\GAL4unspecified.