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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.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
12.916
1.670
29
48
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Tumor-suppressor PTEN; Oxidative stress; Drosophila DJ-1; Cell-death; DJ-1-deficient mice; Tyrosine kinase; In-vivo; Disease; Midbrain; Mouse
Sprache
englisch
Veröffentlichungsjahr
2010
HGF-Berichtsjahr
2010
ISSN (print) / ISBN
1544-9173
e-ISSN
1545-7885
Zeitschrift
PLoS Biology
Quellenangaben
Band: 8,
Heft: 4,
Artikelnummer: e1000349
Verlag
Public Library of Science (PLoS)
Verlagsort
San Francisco
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Developmental Genetics (IDG)
POF Topic(s)
30204 - Cell Programming and Repair
Forschungsfeld(er)
Genetics and Epidemiology
PSP-Element(e)
G-500500-001
G-500500-003
G-500500-003
PubMed ID
20386724
Erfassungsdatum
2010-06-17