Interaction Between Eye Pigment Genes and Tau-Induced Neurodegeneration in Drosophila melanogaster

被引：24

作者：

Ambegaokar, Surendra S. ^{[2
,3
]}

Jackson, George R. ^{[1
,4
,5
]}

机构：

[1] Univ Texas Med Branch, Dept Neurol Neurosci & Cell Biol, Galveston, TX 77555 USA

[2] Univ Calif Los Angeles, Neurosci Interdept Ph D Program, Brain Res Inst,David Geffen Sch Med, Ctr Neurobehav Genet,Semel Inst Neurosci & Human, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, Dept Neurol, David Geffen Sch Med, Los Angeles, CA 90024 USA

[4] Univ Texas Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA

[5] Univ Texas Med Branch, Mitchell Ctr Neurodegenerat Dis, Galveston, TX 77555 USA

来源：

GENETICS | 2010年 / 186卷 / 01期

关键词：

NIEMANN-PICK-DISEASE; ALZHEIMER-LIKE STATE; PHOSPHORYLATION SITES; WHITE GENE; WILD-TYPE; XANTHINE DEHYDROGENASE; PROTEIN-KINASE; HUMAN HOMOLOG; COMPOUND EYE; BINDING;

D O I：

10.1534/genetics.110.119545

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

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-3 beta activity, but not with tau phosphorylation at Ser202/Thr205.

引用

页码：435 / 442

页数：8

共 62 条

[21] Glycogen synthase kinase-3 is associated with neuronal and glial hyperphosphorylated tau deposits in Alzheimer's disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration [J].