Interaction between eye pigment genes and tau-induced neurodegeneration in Drosophila melanogaster.
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.
Ambegaokar
Surendra S
SS
Neuroscience Interdepartmental Ph.D. Program, Brain Research Institute, Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, and Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.
Jackson
George R
GR
D000818:Animals; D029721:Drosophila Proteins / Q000235:genetics* / Q000378:metabolism; D004331:Drosophila melanogaster / Q000201:enzymology / Q000235:genetics* / Q000378:metabolism*; D005123:Eye / Q000378:metabolism* / Q000648:ultrastructure; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D009154:Mutation; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000378:metabolism*; D010641:Phenotype; D010766:Phosphorylation / Q000235:genetics; D010858:Pigmentation / Q000235:genetics*; D016875:tau Proteins / Q000378:metabolism*
D029721:Drosophila Proteins; D016875:tau Proteins; C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; D038362:Glycogen Synthase Kinase 3