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Title
Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila
Issued Date
2015-07
Citation
Cho, Jae Ho. (2015-07). Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila. Biochemical and Biophysical Research Communications, 463(1–2), 1–6. doi: 10.1016/j.bbrc.2015.05.006
Type
Article
Author Keywords
Parkin ; TSPO ; Innate immune response ; VDAC (porin) ; Septic injury ; Wound
Keywords
ACTIVATION ; Amino ACID Sequence ; Animal Experiment ; Animal Model ; Article ; Bacteria (Microorganisms) ; Bacterial Infection ; Bacterial Load ; Comparative Study ; Complementary DNA ; Controlled Study ; DNA Synthesis ; Drosophila ; Gene Interaction ; Heterozygote ; Homozygote ; Hypersensitivity ; Immune Response ; Inflammation ; INNATE IMMUNE-RESPONSES ; Innate Immune Response ; Loss of Function Mutation ; MITOCHONDRIAL QUALITY-CONTROL ; MUTANTS ; MUTATIONS ; Neurodegeneration ; Nonhuman ; Parkin ; Phosphorylation ; Priority Journal ; PROTEIN ; Quantitative Analysis ; Reverse Transcription Polymerase Chain Reaction ; RNA ; RNA Extraction ; Septic Injury ; Sequence Homology ; Survival Rate ; SUSCEPTIBILITY ; Transcription Factor GAL4 ; TSPO ; TSPO Protein ; Tubulin ; Unclassified Drug ; VDac (Porin) ; Voltage Dependent Anion Channel ; Wound ; Wound Healing
ISSN
0006-291X
Abstract

Parkin, an E3 ubuquitin ligase associated with Parkinson's disease (PD), has recently been implicated in mediating innate immunity. However, molecular details regarding parkin-mediated immune response remain to be elucidated. Here, we identified mitochondrial TSPO-VDAC complex to genetically interact with parkin in mediating responses against infection and wound in Drosophila. The loss-of-function mutation in parkin results in defective immune response against bacterial infection. Additionally, parkin mutant larvae showed hypersensitivity against wound regardless of bacterial infection. Interestingly, the combinatorial trans-heterozygotic mutations in parkin and TSPO, or parkin and VDAC showed similar lethal tendency with parkin homozygous mutants. Furthermore, knockdown of TSPO alone also resulted in defective responses to infection and wound analogously to parkin mutants. Taken together, we propose that parkin cooperates with TSPO-VDAC complex to mediate responses against infection and wound. © 2015 Elsevier Inc. All rights reserved.

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URI
http://hdl.handle.net/20.500.11750/2877
DOI
10.1016/j.bbrc.2015.05.006
Publisher
Academic Press Inc.
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Yu, Seong-Woon유성운

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