Abstract
Key scientific discoveries have resulted from genetic studies of Drosophila melanogaster, using a multitude of transgenic fly strains, the majority of which are constructed in a genetic background containing mutations in the white gene. Here we report that white mutant flies from w1118 strain undergo retinal degeneration. We observed also that w1118 mutants have progressive loss of climbing ability, shortened life span, as well as impaired resistance to various forms of stress. Retinal degeneration was abolished by transgenic expression of mini-white+ in the white null background w1118. We conclude that beyond the classical eye-color phenotype, mutations in Drosophila white gene could impair several biological functions affecting parameters like mobility, life span and stress tolerance. Consequently, we suggest caution and attentiveness during the interpretation of old experiments employing white mutant flies and when planning new ones, especially within the research field of neurodegeneration and neuroprotection. We also encourage that the use of w1118 strain as a wild-type control should be avoided.
Highlights
One landmark of modern genetics can be dated to January 1910, when Thomas Hunt Morgan discovered a male of Drosophila melanogaster with white eyes (Morgan, 1910; Green, 1996)
We applied several assays currently used in Drosophila to define neurodegenerative pathologies and found that w− mutant flies suffer from an age-dependent, progressive neurodegenerative retinal phenotype
Retinal degeneration can be precisely monitored in Drosophila by examination of histology sections
Summary
One landmark of modern genetics can be dated to January 1910, when Thomas Hunt Morgan discovered a male of Drosophila melanogaster with white eyes (Morgan, 1910; Green, 1996). The White-Brown dimer transports guanine (Sullivan et al, 1979) and the WhiteScarlet dimer transports tryptophan and kynurenine (Sullivan and Sullivan, 1975), all of which are precursors used for the synthesis of the two eye pigments, drosopterin, and ommochrome (Nolte, 1952) In neurons, these transporters contribute to the synthesis of biogenic amines. W− mutant fruitflies kept in standard laboratory conditions have enhanced light sensitivity (Wu and Wong, 1977) but deficient visual acuity (Kalmus, 1943), contrast and brightness (Wehner et al, 1969), as well as other problems (see Belušic, 2011 for review) Another function of the White protein is to protect retinal photoreceptors from excessive exposure to light (Shoup, 1966; Schraermeyer and Dohms, 1993; Lee and Montell, 2004; Bulgakova et al, 2010). We applied several assays currently used in Drosophila to define neurodegenerative pathologies and found that w− mutant flies suffer from an age-dependent, progressive neurodegenerative retinal phenotype
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