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Pro-survival role for Parkinson's associated gene DJ-1 revealed in trophically impaired dopaminergic neurons.
PLoS Biol. 8:e1000349 (2010)
The mechanisms underlying the selective death of substantia nigra (SN) neurons in Parkinson disease (PD) remain elusive. While inactivation of DJ-1, an oxidative stress suppressor, causes PD, animal models lacking DJ-1 show no overt dopaminergic (DA) neuron degeneration in the SN. Here, we show that aging mice lacking DJ-1 and the GDNF-receptor Ret in the DA system display an accelerated loss of SN cell bodies, but not axons, compared to mice that only lack Ret signaling. The survival requirement for DJ-1 is specific for the GIRK2-positive subpopulation in the SN which projects exclusively to the striatum and is more vulnerable in PD. Using Drosophila genetics, we show that constitutively active Ret and associated Ras/ERK, but not PI3K/Akt, signaling components interact genetically with DJ-1. Double loss-of-function experiments indicate that DJ-1 interacts with ERK signaling to control eye and wing development. Our study uncovers a conserved interaction between DJ-1 and Ret-mediated signaling and a novel cell survival role for DJ-1 in the mouse. A better understanding of the molecular connections between trophic signaling, cellular stress and aging could uncover new targets for drug development in PD.
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Times Cited
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12.916
1.670
29
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Tumor-suppressor PTEN; Oxidative stress; Drosophila DJ-1; Cell-death; DJ-1-deficient mice; Tyrosine kinase; In-vivo; Disease; Midbrain; Mouse
Language
english
Publication Year
2010
HGF-reported in Year
2010
ISSN (print) / ISBN
1544-9173
e-ISSN
1545-7885
Journal
PLoS Biology
Quellenangaben
Volume: 8,
Issue: 4,
Article Number: e1000349
Publisher
Public Library of Science (PLoS)
Publishing Place
San Francisco
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)
POF-Topic(s)
30204 - Cell Programming and Repair
Research field(s)
Genetics and Epidemiology
PSP Element(s)
G-500500-001
G-500500-003
G-500500-003
PubMed ID
20386724
Erfassungsdatum
2010-06-17