Loss of LRRK2/PARK8 induces degeneration of dopaminergic neurons in Drosophila

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Mutations in LRRK2/PARK8 are linked to autosomal dominant forms of Parkinson's disease, but the pathogenic mechanism of LRRK2-associated Parkinson's disease is not fully understood. Moreover, in vivo functions of LRRK2 have not been addressed so far. Thus, we generated and characterized transgenic animals and loss-of-function mutants for LRRK, a sole Drosophila orthologue of human LRRK2. While transgenic expression of pathogenic mutant and wild type LRRK did not show any significant defects, LRRK loss-of-function mutants exhibited severely impaired locomotive activity. Moreover, dopaminergic neurons in LRRK mutants showed a severe reduction in tyrosine hydroxylase immunostaining and shrunken morphology, implicating their degeneration in the mutants. Collectively, our findings unprecedentedly show in vivo that LRRK2 is critical for the integrity of dopaminergic neurons and intact locomotive activity in Drosophila. (C) 2007 Elsevier Inc. All rights reserved.
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Issue Date
2007-06
Language
English
Article Type
Article
Keywords

PARKINSONS-DISEASE; LRRK2 G2019S; MUTATIONS; LOCALIZATION; PATHOLOGY; MUTANTS; BRAIN

Citation

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.358, no.2, pp.534 - 539

ISSN
0006-291X
DOI
10.1016/j.bbrc.2007.04.156
URI
http://hdl.handle.net/10203/2258
Appears in Collection
BS-Journal Papers(저널논문)
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