Abstract
Null mutations in the genes white and brown, but not scarlet, enhance a rough eye phenotype in a Drosophila melanogaster model of tauopathy; however, adding rosy mutations suppresses these effects. Interaction with nucleotide-derived pigments or increased lysosomal dysregulation are potential mechanisms. Finally, tau toxicity correlates with increased GSK-3β activity, but not with tau phosphorylation at Ser202/Thr205.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Drosophila Proteins / genetics*
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Drosophila Proteins / metabolism
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Drosophila melanogaster / enzymology
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Drosophila melanogaster / genetics*
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Drosophila melanogaster / metabolism*
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Eye / metabolism*
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Eye / ultrastructure
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Glycogen Synthase Kinase 3 / metabolism
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Glycogen Synthase Kinase 3 beta
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Mutation
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Neurodegenerative Diseases / genetics
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Neurodegenerative Diseases / metabolism*
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Phenotype
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Phosphorylation / genetics
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Pigmentation / genetics*
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tau Proteins / metabolism*
Substances
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Drosophila Proteins
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tau Proteins
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GSK3B protein, human
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Glycogen Synthase Kinase 3 beta
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Glycogen Synthase Kinase 3