1. Neuroscience

Parkinson’s disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss

  1. Lorenzo Ghezzi
  2. Sabine Kuenen
  3. Ulrike Pech
  4. Nils Schoovaerts
  5. Ayse Kilic
  6. Suresh Poovathingal
  7. Kristofer Davie
  8. Jochen Lamote
  9. Roman Praschberger  Is a corresponding author
  10. Patrik Verstreken  Is a corresponding author
  1. VIB-KU Leuven Center for Neuroscience, Belgium
  2. KU Leuven, Department of Neurosciences, Leuven Brain Institute, Belgium
  3. VIB-KU Leuven Center for Neuroscience, Single Cell and Microfluidics Expertise Unit, Belgium
  4. VIB-KU Leuven Center for Neuroscience, Single Cell Bioinformatics Unit, Belgium
  5. VIB Flow Core Leuven, VIB Technologies, Belgium
  6. Medical University of Innsbruck, Institute of Human Genetics, Austria
https://doi.org/10.7554/eLife.105386.3
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Cite this article
  1. Lorenzo Ghezzi
  2. Sabine Kuenen
  3. Ulrike Pech
  4. Nils Schoovaerts
  5. Ayse Kilic
  6. Suresh Poovathingal
  7. Kristofer Davie
  8. Jochen Lamote
  9. Roman Praschberger
  10. Patrik Verstreken
(2026)
Parkinson’s disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss
eLife 14:RP105386.
https://doi.org/10.7554/eLife.105386.3
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5 figures, 1 table and 4 additional files

Figures

Figure 1 with 1 supplement
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Ensheathing glia (EG) are affected non-cell autonomously by Pink1 loss-of-function (with Figure 1—figure supplement 1).

(A) tSNE of the cells of Pink1P399L knock-in mutants (5-day-old). Cell types are labeled with colors, indicating the number of deregulated genes compared to control. EG are encircled and labeled. (B–B”) Maximum intensity projections of confocal images of fly brains (5±1-day-old) stained with anti-GFP (green) and anti-Brp (magenta), where anti-GFP marks EG and anti-Brp marks presynaptic sites of the antennal lobes in flies where CD8GFP is expressed via the EG driver MZ709-Gal4. Scale bar: 20 µm. (B’) Maximum intensity projection of confocal images of controls vs. controls 24 hr after olfactory receptor neuron (ORN)-severing (injury). (B”) Maximum intensity projection of confocal images of Pink1KO-WS/y vs. Pink1KO-WS/y 24 hr after ORNs severing (injury). (C) Quantification of GFP intensity within the glomeruli of the antennal lobe area, region of interest (ROI), in 5±1-day-old flies (as in B) relative to controls. ANOVA with Dunnett’s multiple comparison test, * is p<0.05, *** is p<0.001. Effect size: η2=0.23. Bars: mean ± SD; points are individual animals, N≥13 per genotype, 4 replicates. (D–D”) Maximum intensity projection of confocal images of fly brains (5±1-day-old) stained with anti-GFP (green) and anti-Brp (magenta), where anti-GFP marks EG and anti-Brp marks presynaptic sites of the antennal lobes in flies where CD8GFP is expressed via the EG driver MZ709-Gal4. Scale bar: 20 µm. (D’) Maximum intensity projection of confocal images of control (w1118) and Pink1KO-WS/y animals. (D”) Maximum intensity projection of confocal images of animals with Pink1 downregulation in EG and Pink1KO-WS/y with Pink1 rescued in EG. (E) Quantification of GFP intensity within the glomeruli of the antennal lobe area in 5-day-old flies (as in D) relative to controls. ANOVA with Tukey’s multiple comparison test, ** is p<0.01, *** is p<0.001. **** is p<0.0001. Effect size: η2=0.36. Bars: mean ± SD; points are individual animals, N≥10 per genotype, 4 replicates.

Figure 1—figure supplement 1
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Representative confocal image of a 5±1-day-old MZ709-Gal4>UAS-His2Av::eGFP brain stained with anti-GFP (cyan) and anti-ELAV (magenta).

Scale bar: 50 µm; N=3, 1 replicate.

Figure 2 with 1 supplement
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Pink1 in ensheathing glia (EG) is necessary to support synaptic integrity (with Figure 2—figure supplement 1).

(A) Representative electroretinogram (ERG) traces of indicated genotypes: ON peak is highlighted by the arrow. (B) Normalized ON peak amplitude of flies (5±1-day-old). ANOVA with Tukey’s multiple comparison test, ns is p>0.05, ** is p<0.01, **** is p<0.0001. Effect size: η2=0.55. Bars: mean ± SD; points are individual animals, N≥11 per genotype, 3 replicates. (C–C”) (C) Maximum intensity projection of confocal images of control and Pink1KO-WS/y in mushroom bodies (MBs) of aged flies (22±2-day-old), stained with anti-TH (cyan) and anti-DLG (magenta) antibodies – DLG is used to mark post-synaptic sites of MBs. The black-and-white image is the middle Z-plane within the region of interest of the MB (region of interest [ROI], yellow), which is used to represent the thresholded TH area (white). Scale bar: 20 µm. (C’) Maximum intensity projection of confocal images of w1118 with Pink1 downregulation in EG. (C”) Maximum intensity projection of confocal images of Pink1KO-WS/y with Pink1 rescued in EG. (D) Quantification of the dopaminergic synaptic area at MB neuropil in aged flies (22±2-day-old). ANOVA with Tukey’s multiple comparison test, ns is p>0.05, *** is p<0.001. Effect size: η2=0.38. Bars: mean ± SD; points are individual animals, N≥12 per genotype, 3 replicates.

Figure 2—figure supplement 1
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Examples of confocal Z-stacks of anti-DLG-labeled fly brains (22±2-day-old) of the indicated genotypes.

Such images were used to delineate regions of interest (ROIs) to quantify DAN innervation onto the mushroom bodies (MBs). (A) Control (w1118/y;; MZ709-Gal4/+); (B) Pink1KO-WS/y;; MZ709-Gal4/+; (C) flies where Pink1 is downregulated in EG (w1118/y;; MZ709-Gal4/Pink1RNAi); (D) Pink1KO-WS/y flies with expression of wild-type Pink1 in EG (Pink1KO-WS/y;; MZ709-Gal4/UAS-Pink1). Scale bar: 20 µm.

Figure 3
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Cell-type-specific transcriptomics reveals modifiers of neuronal dysfunction.

(A) Scheme of cell-type-specific transcriptomics (Created in BioRender. Verstreken, P. (2025) https://biorender.com/p56u250). (B) Scaled gene expression of representative genes for ensheathing glia (EG) and neurons after sorting EG or neurons using the protocol described in (A). N=2, 2 replicates. (C) Differentially expressed genes (DEGs) in EG in Pink1KO-WS/y compared to control flies, plotted according to their log2foldchange and the –log10 of the adjusted p-value. Intercept in red (–log10 adjusted p-value = 4.31); light green dots are all detected genes, dark green are the 50 most deregulated genes, and the pink dot is from a gene positive in the genetic screen in (D). *Two data points are outside the boundaries of the plot. To determine the transcriptomic profile of each genotype, N=3 independent repeat experiments were used, with 3 replicates each time. (D) Electroretinogram (ERG) ON peak value differences of control (red) and of Pink1KO-WS/y flies (5±1-day-old) with DEGs downregulated or upregulated, specifically in EG relative to Pink1KO-WS/y. ANOVA with Dunnett’s test, * is p<0.05, ** is p<0.01, **** is p<0.0001. Effect size: η2=0.44. Bars: mean ± SD; points are individual animals, N≥3 per genotype. *One data point is outside the boundaries of the plot.

Figure 4 with 1 supplement
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Vps35 and Vps13 downregulation in ensheathing glia (EG) rescues synaptic deficits in Pink1KO-WS-y flies (with Figure 4—figure supplement 1).

(A) Representative electroretinogram (ERG) traces of control, Pink1KO-WS/y flies, and Pink1KO-WS/y flies with Vps35 or Vps13 downregulated in EG. (B) Quantification of the normalized ON peak response of flies with the genotypes in (A) (5±1-day-old). ANOVA with Dunnett’s multiple comparison test, ns is p>0.05, ** is p<0.01. Effect size: η2=0.48. Bars: mean ± SD; points are individual animals, N≥10 per genotype, 3 replicates. (C) Maximum intensity projection of confocal images of mushroom bodies (MBs) of aged flies (22±2-day-old) of control, Pink1KO-WS/y, and Pink1KO-WS/y with Vps13 downregulated in EG , labeled with anti-TH (cyan) and anti-DLG (magenta); DLG is used to mark the MB neuropil. The black-and-white image is the middle Z-plane within the region of interest of the MB (regions of interest [ROI], yellow), which is used to represent the thresholded TH area (white). Scale bar: 20 µm. (D) Quantification of the dopaminergic synaptic area within MB of aged flies (22±2-day-old). ANOVA with Dunnett’s multiple comparison test, ns is p>0.05, *** is p<0.001. Effect size: η2=0.23. Bars: mean ± SD; points are individual animals, n≥22 per genotype, 5 replicates.

Figure 4—figure supplement 1
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Examples of confocal Z-stacks of anti-DLG labeled fly brains (22±2-day-old) of the indicated genotypes.

Such images were used to delineate regions of interest (ROIs) to quantify dopaminergic neuron (DAN) innervation onto the mushroom bodies (MBs). (A) Control (w1118/y;; MZ709-Gal4/+); (B) Pink1KO-WS/y;; MZ709-Gal4/+; (C) Pink1KO-WS/y flies with Vps13 downregulation in ensheathing glia (EG) (Pink1KO-WS/y;; Vps13RNAi/MZ709-Gal4). Scale bar: 20 µm.

Figure 5
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Modulation of endoplasmic reticulum (ER)-mitochondria contact sites and lipid transfer in ensheathing glia (EG) rescues Pink1-dependent neuronal dysfunction.

Schematic representation of the suggested model (Created with BioRender.com). (A) Loss of Pink1 leads to an abnormal increase in endoplasmic reticulum (ER)-mitochondria contact sites (represented by blue thick lines), resulting in enhanced ER-to-mitochondria lipid transfer and dysregulation of ER lipid composition (represented by yellow lipids). Increased organelle membrane contacts and lipid flux in EG contribute to neuronal dysfunction in a non-cell-autonomous manner. (B) Genetic downregulation of ER-mitochondria contact and lipid transfer regulators in EG rescues Pink1-induced neuronal phenotypes through two convergent mechanisms. Reduction of Vps35 may decrease the number of ER-mitochondria contact sites, possibly via MUL1-mediated Mitofusin (Mfn) turnover, potentially normalizing calcium and lipid homeostasis. In parallel, downregulation of Vps13, a lipid transfer facilitator at organelle contact sites, limits ER-to-mitochondria lipid transfer capacity, counteracting the excessive lipid flux induced by Pink1 loss. Both interventions restore organelle homeostasis in EG and result in rescue of neuronal dysfunction through a non-cell-autonomous mechanism. Rescue of neuronal dysfunction by EG-specific Vps35RNAi was demonstrated in the visual system (electroretinogram [ERG] on-transient; Figure 4A and B). Whether this extends to dopaminergic synaptic loss, as demonstrated for Vps13 (Figure 4C and D), has not yet been examined and may be cell-type- and/or phenotype-specific.

Tables

Appendix 1—key resources table
Reagent type (species) or resourceDesignationSource or referenceIdentifiersAdditional information
AntibodyRabbit polyclonal anti-GFPThermo Fisher ScientificCat#A-11122; RRID:AB_221569(1:1000)
AntibodyMouse monoclonal anti-BrpDSHBCat#nc82; RRID:AB_2314866(1:100)
AntibodyMouse monoclonal anti-DLGDSHBCat#4F3; RRID:AB_528203(1:100)
AntibodyRabbit polyclonal anti-THSigma-AldrichCat#AB 152(1:200)
AntibodyAlexa Fluor 488 goat anti-rabbitInvitrogenCat#A11034(1:1000) in invasion phenotype, (1:500) in TH staining
AntibodyAlexa Fluor 555 goat anti-mouse IgG2aInvitrogenCat#A21137(1:1000) in invasion phenotype, (1:500) in TH staining
Commercial assay, kitAgencourt AMPure XPBeckman CoulterCat#A63880
Commercial assay, kitKAPA HiFi HotStart ReadyMixRocheCat#07958927001
Commercial assay, kitNextera XT DNA Library Preparation KitIlluminaCat#FC-131-1096
Peptide, recombinant proteinDispase ISigma-AldrichCat#D4818
Peptide, recombinant proteinCollagenase IThermo Fisher ScientificCat#17100017
Peptide, recombinant proteinSuperScript II Reverse TranscriptaseThermo Fisher ScientificCat#18064022
Chemical compound, drugTrypsin-EDTA (0.5%)Thermo Fisher ScientificCat#15400054
Chemical compound, drugTriton X-100 SolutionSigma-AldrichCat#93443-100Ml
Chemical compound, drugParaformaldehydeSigma-AldrichCat#252549
Chemical compound, drugActinomycin DSigma-AldrichCat#A1410
Chemical compound, drugEDTASigma-AldrichCat#E6511
Chemical compound, drugDAPISigma-AldrichCat#D9542
Chemical compound, drugMgCl2 (1 M)Thermo Fisher ScientificCat#AM9530G
Chemical compound, drugRNaseOUTThermo Fisher ScientificCat#10777019
Chemical compound, drugBetaineSigma-AldrichCat#B0300
Chemical compound, drugDTT (100 mM Solution)Thermo Fisher ScientificCat#707265ML
Chemical compound, drugBuffer EBQIAGENCat#19086
Chemical compound, drugRapiClear 1.47Sunjin LabCat#RC147001
Sequence-based reagentdNTP MixPromegaCat#U1511
Sequence-based reagentPrimers, gRNAs, oligos, gBlocksIntegrated DNA Technologies (IDT)
Strain background (D. melanogaster)w[1118] (w1118)Kaempf et al., 2026NA
Strain background (D. melanogaster)w[1118] M{w+} (w1118 w+)Kaempf et al., 2026NA
Genetic reagent (D. melanogaster)w[1118] TI{w[+]=white-STAR}Pink1[KO-WS]/FM7a (Pink1KO-WS/y)Kaempf et al., 2026NA
Genetic reagent (D. melanogaster)Yw;; UAS-His2Av::eGFP.VK27/TM3Sb (UAS- His2Av::eGFP)This studyNA
Genetic reagent (D. melanogaster);;MZ0709-Gal4Ito et al., 1995NA
Genetic reagent (D. melanogaster)y[1] w[*]; P{w[+mC]=UAS-mCD8::GFP.L}LL5, P{UAS-mCD8::GFP.L}2 (UAS-mCD8-GFP)Lee and Luo, 1999BDSC_5137
Genetic reagent (D. melanogaster)w[*]; P{y[+t7.7] w[+mC]=GMR-56-GAL4}attP24/CyO (GMR-56-Gal4)Jenett et al., 2012BDSC_77469
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF01672}attP2 (Pink1RNAi)Perkins et al., 2015BDSC_31170
Genetic reagent (D. melanogaster)w[*]; P{w[+mC]=UAS-Pink1.C}A (UAS-Pink1)Bloomington Drosophila Stock CenterBDSC_51648
Genetic reagent (D. melanogaster)w[1118]; P{y[+t7.7] w[+mC]=GMR57C10-GAL4}attP2 (nSyb-Gal4)Jenett et al., 2012BDSC_39171
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01715}attP40 (Vps13RNAi)Perkins et al., 2015BDSC_38270
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01858}attP40 (Vps35RNAi)Perkins et al., 2015BDSC 38944
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS05488}attP40 (CG17660RNAi)Perkins et al., 2015BDSC_67022
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF03249}attP2 (ProcRNAi)Perkins et al., 2015BDSC_29570
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC05229}attP40 (fizRNAi)Perkins et al., 2015BDSC_62222
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF01165}attP2 (CG15011RNAi)Perkins et al., 2015BDSC_31589
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC04857}attP40 (CG17612RNAi)Perkins et al., 2015BDSC_57540
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC05717}attP40 (PrpkRNAi)Perkins et al., 2015BDSC_64844
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ22434}attP40 (LnpkRNAi)Perkins et al., 2015BDSC_64036
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01827}attP2 (PIG-BRNAi)Perkins et al., 2015BDSC_38359
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01840}attP2/TM3, Sb[1] (spagRNAi)Perkins et al., 2015BDSC_38371
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS00070}attP2 (RelRNAi)Perkins et al., 2015BDSC_33661
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC04640}attP40 (Atac1RNAi)Perkins et al., 2015BDSC_57250
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.GLV21056}attP2 (l(3)07882RNAi)Perkins et al., 2015BDSC_35691
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS00529}attP2 (PldRNAi)Perkins et al., 2015BDSC_32839
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS02243}attP2 (Rpp25RNAi)Perkins et al., 2015BDSC_41679
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMC03184}attP40 (GMFRNAi)Perkins et al., 2015BDSC_51452
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01358}attP2/TM3, Sb[1] (Atg7RNAi)Perkins et al., 2015BDSC_34369
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ03126}attP40 (Ada2aRNAi)Perkins et al., 2015BDSC_50905
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC06224}attP2 (CG12773RNAi)Perkins et al., 2015BDSC_65949
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS00328}attP2 (CG7627RNAi)Perkins et al., 2015BDSC_32337
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMS00870}attP2 (DarkRNAi)Perkins et al., 2015BDSC_33924
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF03275}attP2 (CG3703RNAi)Perkins et al., 2015BDSC_29596
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMS01175}attP2/TM3, Sb[1] (NiPp1RNAi)Perkins et al., 2015BDSC_34696
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ22813}attP40 (CG31370RNAi)Perkins et al., 2015BDSC_60456
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ23526}attP40 (IrbpRNAi)Perkins et al., 2015BDSC_61942
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF02313}attP2 (CG32532RNAi)Perkins et al., 2015BDSC_26750
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ30013}attP40/CyO (RhauRNAi)Perkins et al., 2015BDSC 62936
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HM05047}attP2 (hfwRNAi)Perkins et al., 2015BDSC_28561
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.JF02192}attP2 (achiRNAi)Perkins et al., 2015BDSC_31903
Genetic reagent (D. melanogaster)y[1] v[1]; P{y[+t7.7] v[+t1.8]=TRiP.HMJ23972}attP40/CyO (TTLL6ARNAi)Perkins et al., 2015BDSC_62488
Genetic reagent (D. melanogaster)y[1] sc[*] v[1] sev[21]; P{y[+t7.7] v[+t1.8]=TRiP.HMC03076}attP2 (NosRNAi)Perkins et al., 2015BDSC_50675
Genetic reagent (D. melanogaster)w[1118]; P{w[+mC]=UAS-Nos.L}2 (UAS-Nos)Bloomington Drosophila Stock CenterBDSC_56823
Recombinant DNA reagentpUASTattBBischof et al., 2007https://www.flyc31.org
Software, algorithmFijiSchindelin et al., 2012RRID:SCR_002285https://imagej.net/Fiji
Software, algorithmGraphPad PrismGraphPad SoftwareRRID:SCR_002798https://www.graphpad.com/scientific-software/prism/
Software, algorithmPython (v3.7.3)PythonRRID:SCR_008394http://www.python.org/
Software, algorithmscanpyWolf et al., 2018RRID:SCR_018139https://github.com/theislab/scanpy
Software, algorithmDESeq2Love et al., 2014RRID:SCR_015687https://bioconductor.org/packages/release/bioc/html/DESeq2.html
Software, algorithmClampfitMolecular Deviceshttps://www.moleculardevices.com
Software, algorithmAxoscopeMolecular Deviceshttps://www.moleculardevices.com
Software, algorithmIgor ProWaveMetricsRRID:CR_000325https://www.wavemetrics.com/products/ igorpro/igorpro.htm
Software, algorithmFACSDiva software v9.0.1BD BiosciencesRRID:SCR_001456https://www.bdbiosciences.com/en-be/products/software/instrument-software/bd-facsdiva-software
Software, algorithmnf-core/rnaseqPatel et al., 2020https://nf-co.re/rnaseq/3.14.0/
Software, algorithmfastpChen et al., 2018RRID:SCR_016962https://github.com/OpenGene/fastp
Software, algorithmRStudioRStudio, PBC/Posit
Software, algorithmBioRenderBioRenderhttps://BioRender.com
Software, algorithmSTARDobin et al., 2013RRID:SCR_004463https://github.com/alexdobin/STAR
Software, algorithmHarmonyKorsunsky et al., 2019RRID:SCR_022206https://github.com/immunogenomics/harmony

Additional files

Supplementary file 1

Differentially expressed genes (DEGs) in ensheathing glia (EG) identified by cell-type-specific transcriptomics.

https://cdn.elifesciences.org/articles/105386/elife-105386-supp1-v1.pdf
Supplementary file 2

Complete list of Drosophila melanogaster genotypes used in this study.

https://cdn.elifesciences.org/articles/105386/elife-105386-supp2-v1.xlsx
MDAR checklist
https://cdn.elifesciences.org/articles/105386/elife-105386-mdarchecklist1-v1.docx
Source data 1

Numerical source data for Figures 1—4.

https://cdn.elifesciences.org/articles/105386/elife-105386-data1-v1.xlsx

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  1. Lorenzo Ghezzi
  2. Sabine Kuenen
  3. Ulrike Pech
  4. Nils Schoovaerts
  5. Ayse Kilic
  6. Suresh Poovathingal
  7. Kristofer Davie
  8. Jochen Lamote
  9. Roman Praschberger
  10. Patrik Verstreken
(2026)
Parkinson’s disease-associated PINK1 loss disrupts ensheathing glia and causes dopaminergic neuron synapse loss
eLife 14:RP105386.
https://doi.org/10.7554/eLife.105386.3