Articles by Patrik Verstreken in JoVE
In Vivo Single-Molecule Tracking at the Drosophila Presynaptic Motor Nerve Terminal Adekunle T. Bademosi1, Elsa Lauwers2, Rumelo Amor3, Patrik Verstreken2, Bruno van Swinderen3, Frédéric A. Meunier1 1Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, 2VIB Centre for Brain and Disease Research, KU Leuven Department of Neurosciences, Leuven Institute for Neurodegenerative Disease (LIND), 3Queensland Brain Institute, The University of Queensland Here we illustrate how single molecule photo-activated localization microscopy can be carried out on the motor nerve terminal of a live Drosophila melanogaster third instar larva.
Other articles by Patrik Verstreken on PubMed
Cardiolipin Promotes Electron Transport Between Ubiquinone and Complex I to Rescue PINK1 Deficiency The Journal of Cell Biology. | Pubmed ID: 28137779 PINK1 is mutated in Parkinson's disease (PD), and mutations cause mitochondrial defects that include inefficient electron transport between complex I and ubiquinone. Neurodegeneration is also connected to changes in lipid homeostasis, but how these are related to PINK1-induced mitochondrial dysfunction is unknown. Based on an unbiased genetic screen, we found that partial genetic and pharmacological inhibition of fatty acid synthase (FASN) suppresses toxicity induced by PINK1 deficiency in flies, mouse cells, patient-derived fibroblasts, and induced pluripotent stem cell-derived dopaminergic neurons. Lower FASN activity in PINK1 mutants decreases palmitate levels and increases the levels of cardiolipin (CL), a mitochondrial inner membrane-specific lipid. Direct supplementation of CL to isolated mitochondria not only rescues the PINK1-induced complex I defects but also rescues the inefficient electron transfer between complex I and ubiquinone in specific mutants. Our data indicate that genetic or pharmacologic inhibition of FASN to increase CL levels bypasses the enzymatic defects at complex I in a PD model.
Neurons Eat Glutamate to Stay Alive The Journal of Cell Biology. | Pubmed ID: 28298409 Neurons are thought to primarily rely on glucose to fuel mitochondrial metabolism. In this issue, Divakaruni et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201612067) show that neurons are also happy to use glutamate. When neurons use this neurotransmitter, its concentration drops, thus protecting against glutamate-induced excitotoxic stress.
α-Synuclein and Tau: Mitochondrial Kill Switches Neuron. | Pubmed ID: 29301103 α-Synuclein resides in Lewy bodies in Parkinson's disease. Ordonez et al. (2017) now show that α-syn disrupts the actin network, causing Drp1-dependent mitochondrial fission defects. This is similar to defects induced by the PD risk factor Tau, suggesting converging pathways in neurodegeneration.