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Inhibition of the deubiquitinase USP8 corrects a Drosophila PINK1 model of mitochondria dysfunction
Abstract
Aberrant mitochondrial dynamics disrupts mitochondrial function and contributes to disease conditions. A targeted RNA interference screen for deubiquitinating enzymes (DUBs) affecting protein levels of multifunctional mitochondrial fusion protein Mitofusin (MFN) identified USP8 prominently influencing MFN levels. Genetic and pharmacological inhibition of USP8 normalized the elevated MFN protein levels observed in PINK1 and Parkin-deficient models. This correlated with improved mitochondrial function, locomotor performance and life span, and prevented dopaminergic neurons loss in Drosophila PINK1 KO flies. We identified a novel target antagonizing pathologically elevated MFN levels, mitochondrial dysfunction, and dopaminergic neuron loss of a Drosophila model of mitochondrial dysfunction.
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USP8 down-regulation or pharmacological inhibition ameliorates the phenotype of PINK1 and Parkin KO flies by preventing neurodegeneration and rescues mitochondrial defects, lifespan and locomotor dysfunction.
“We also previously demonstrated that USP8 down-regulation or its pharmacological inhibition ameliorates the phenotype of PINK1 and Parkin KO flies by preventing neurodegeneration and rescues mitochondrial defects, lifespan and locomotor dysfunction in these flies [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
USP8 down-regulation or pharmacological inhibition ameliorates the phenotype of PINK1 and Parkin KO flies.
“and its down-regulation or pharmacological inhibition ameliorates the phenotype of PINK1 and Parkin KO flies [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
Mitochondrial respiration and Complex I activity are not affected in USP8-down-regulating conditions.
“our previous study showed that mitochondrial respiration and Complex I activity are not affected in USP8-down-regulating conditions [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
Mitochondrial degradation induced by USP8 down-regulation may be compensated for by productive mitochondrial biogenesis.
“Because the reduction in mitochondrial content is quite modest, and USP8 downregulating cells do not display any defects in mitochondrial respiration [20], it is possible that mitochondrial degradation induced by USP8 down-regulation is compensated for by productive mitochondrial biogenesis.”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
The morphological change of increased mitochondrial fission likely facilitates mitochondrial quality control.
“Thus, this morphological change likely facilitates quality control, whereas it does not seem to affect mitochondrial functionality, in that our previous study showed that mitochondrial respiration and Complex I activity are not affected in USP8-down-regulating conditions [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
USP8-deficient flies did not show any particular detrimental phenotypes and mitochondrial functionality remained intact.
“Importantly, USP8-deficient flies did not show any particular detrimental phenotypes and mitochondrial functionality remained intact [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
USP8-deficient cells do not display defects in mitochondrial respiration, nor loss of mitochondrial membrane potential to trigger PINK1/Parkin activation.
“Our previous studies showed that USP8-deficient cells do not display any defects in mitochondrial respiration, nor loss of mitochondrial membrane potential to trigger PINK1/Parkin activation [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
The decreased mitochondrial aspect ratio in USP8-down-regulating flies supports the previous observation that USP8-down-regulating S2R+ cells display fragmented mitochondria.
“These results fully support what we previously observed in USP8-down-regulating S2R+ cells that displayed fragmented mitochondria [20].”
From USP8 Down-Regulation Promotes Parkin-Independent Mitophagy in the Drosophila Brain and in Human Neurons (2023) · cites this paper as [20]
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Citations
Cites
Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin
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The Mitochondrial Fusion-Promoting Factor Mitofusin Is a Substrate of the PINK1/Parkin Pathway
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Metadata
- Authors
- von Stockum, S., Sanchez-Martinez, A., Corrà, S., Chakraborty, J., Marchesan, E., Locatello, L., Da Rè, C., Cusumano, P., Caicci, F., Ferrari, V., Costa, R., Bubacco, L., Rasotto, M. B., Szabo, I., Whitworth, A. J., Scorrano, L., & Ziviani, E.
- Affiliations
- Fondazione Ospedale San Camillo, IRCCS, Venezia, Italy
- MRC Mitochondrial Biology Unit, Cambridge Biomedical Campus, Cambridge, UK
- Department of Biology, University of Padova, Padova, Italy
- Venue
- Life Science Alliance
- Publisher
- Life Science Alliance, LLC
- Published
- 2019-04
- Volume
- 2
- Issue
- 2
- Pages
- e201900392
- ISSN
- 2575-1077
- PMC
- PMC6467245
- Cited by
- 30
- References
- 10
- Language
- en
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