Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila
- Title
- Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila
- Author(s)
- Cho, Jae Ho ; Park, Jeong Hyang ; Chung, Chang Geon ; Shim, Hyun-Jung ; Jeon, Keun Hye ; Yu, Seong-Woon ; Lee, Sung Bae
- Issued Date
- 2015-07
- Citation
- Biochemical and Biophysical Research Communications, v.463, no.1-2, pp.1 - 6
- 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.
- Publisher
- Academic Press Inc.
- Related Researcher
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Yu, Seong-Woon
- Research Interests Molecular mechanisms of neuronal cell death and neurodegeneration
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