|Feature type||allele||Associated gene||Dmel\rdgC|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
rdgC mutant larvae show a statistically significant increase in the preference for 18[o]C.
Mutant flies show a decrease in the amplitude of the electroretinogram (ERG) compared to wild type.
The reduction in electroretinogram (ERG) amplitude seen in flies exposed to constant light is accelerated by rdgC306.
rdgC306 animals kept in the dark for 6 days show normal ommatidial structure and highly ordered rhabdomeric structure typical of healthy photoreceptors, but animals 6 days after a single 10 minute exposure to blue light show extensive disorganisation of ommatidial structure and morphological changes in photoreceptor cells that are characteristic of apoptosis. Vesiculation and disassembly of the rhabdomeric membrane in the R1-R6 cells, and in some cases encasement of the rhabdomere by phagocytotic cells. The rhabdomere of the UV-sensitive R7 cell is unaffected. In contrast to blue-light stimulated animals, mutants 6 days after 10 min blue immediately followed by 10 min orange light exposures are indistinguishable from unstimulated animals. Photoreceptor cells in mutants stimulated by blue light and kept in the dark for 3 days show slightly smaller rhabdomeres, but little evidence of photoreceptor pathology. In contrast, a full blown picture of apoptosis is evident after 6 days. A 10 minute pulse of orange light 3 days after blue light stimulus followed by three additional days of dark shows complete suppression of apoptosis. Mutants exposed to 10 minutes of blue light followed by 4 days of dark incubation show elimination of the Deep Pseudopupil.
Ommatidia, after light-rearing for 8 weeks, show the typical features of apoptosis: cytoplasmic condensation, nuclear chromatin condensation and relatively normal looking mitochondria.
Light-dependent retinal degeneration. ERGs and intracellular recordings demonstrate mutant photoreceptors exhibit a notable decrease in the rate of deactivation relative to control flies. Mutants exhibit a prolonged afterpotential (PDA) defect, this is also rescued by ninaEΔ356.
Third instar foraging larvae show negative photobehaviour indistinguishable from the wild-type response to light. Third instar larvae show a decrease in negative phototaxis from the onset of wandering culminating in random photobehaviour indistinguishable from the response of wild-type larvae.
Ultrastructural analysis of photoreceptor degeneration demonstrates that the histological and physiological deficits result from degeneration triggered by light.
|Phenotype Manifest In|
The light dependant retinal degeneration seen in Gα49B1, rdgC306 animals is strongly suppressed by Arr23. The addition of Gα49B1 and Arr21 to rdgC306 show a rapid degeneration of photoreceptor cells. The addition of rdgC306 to Gα49B1 flies undergo a dramatic and rapid loss of Deep Pseudopupils (DPPs) between days 4 and 6 of days of light exposure. This phenotype is partially rescued by the addition of Arr23, and enhanced (the numbers of DPPs start to reduce immediately on exposure to light) by the addition of Arr21. rdgC306,shi1 mutants exposed to 10 minutes of blue light followed by 4 days of dark incubation show a partial rescue of the Deep Pseudopupil phenotype seen in rdgC306 flies alone.
Light-induced retinal degeneration is blocked by expression of BacA\p35GMR.PH: photoreceptor cells and organelles are indistinguishable from wild-type. The 'walking optomotor response' for rdgC306/BacA\p35GMR.PH flies is normal.
|Complementation & Rescue Data|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 16 )|