Biochemical and Biophysical Research Communications
The PINK1–Parkin pathway is involved in the regulation of mitochondrial remodeling process
Section snippets
Materials and methods
Fly stocks. The generation of park1 mutants, UAS-parkin, PINK1B9 mutants and UAS-PINK1 has been previously described in [16] and [9], respectively. We have generated UAS-drp1 and UAS-drp1K38A (both C-terminally HA-tagged), UAS-opa1 (C-terminally Flag-tagged) and UAS-marf (C-terminally Flag-tagged) transgenic lines, and their expression was confirmed by immunoblot analysis. opa1EP (opa1p{EPgy2}CG8479) [14] and drp12[13] lines were obtained from Dr. A. Mcquibban (University of Toronto) and Dr. H.
Results and discussion
We and others have previously found that DrosophilaPINK1 and parkin mutants show mitochondrial swelling in the indirect flight muscle [9], [10], [11], so we sought to observe the mitochondrial morphology when both PINK1 and Parkin are overexpressed. Coexpression of PINK1 and Parkin under the hs-GAL4 driver resulted in pupal lethality when raised at 25 °C, but at 18 °C several adult escapees came out and we found smaller mitochondria in the indirect flight muscle compared to the control (Fig. 1A).
Funding
This research was supported by a National Creative Research Initiatives Grant (R16-2001-002-01001-0) from Korean Ministry of Education, Science and Technology/KOSEF.
Conflicts of interest
The authors declare no competing financial interests.
Acknowledgments
We are grateful to Drs. A. Mcquibban, H. J. Bellen, S. Birman, for providing us fly stocks. We also thank Chung’s laboratory members for helpful discussions.
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2023, Biochemical and Biophysical Research CommunicationsUpregulation of the Autophagy Adaptor p62/SQSTM1 Prolongs Health and Lifespan in Middle-Aged Drosophila
2019, Cell ReportsCitation Excerpt :To do so, we directly manipulated Drp1, a dynamin-related protein that promotes mitochondrial fission (Hoppins et al., 2007). More specifically, we inhibited mitochondrial fission, by inducing a dominant-negative Drp1 (Drp1K38A) transgene (Park et al., 2009), from midlife onward in flies with increased dp62 levels and examined the impact on mitochondrial morphology, mitochondrial function, and compared survivorship to flies with increased dp62 alone. We confirmed that inducing dominant-negative Drp1 (Drp1K38A) from midlife onward in flies with increased dp62 levels (Figure S7A) prevented an increase in mitochondrial fission (Figures 6A and 6B; quantification in Figure 6C).