ArticleMolecular biology of the cell2018
Phosphorylation of MCAD selectively rescues PINK1 deficiencies in behavior and metabolism.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Rewiring Lipid Metabolism: PINK1 as a Central Regulator of Mitochondrial Homeostasis in Parkinson's Disease.International journal of molecular sciences · 2026Review
- The MIRO1-BAX Complex Dictates Life and Death at the Mitochondrial Gate.bioRxiv : the preprint server for biology · 2026Article
- Characterizing fatty acid oxidation genes in Drosophila.G3 (Bethesda, Md.) · 2025Article
- Regulatory changes in the fatty acid elongase eloF underlie the evolution of sex-specific pheromone profiles in Drosophila prolongata.BMC biology · 2025Article
- Regulatory Changes in the Fatty Acid ElongasebioRxiv : the preprint server for biology · 2024Article
- A gene therapy targeting medium-chain acyl-CoA dehydrogenase (MCAD) did not protect against diabetes-induced cardiac pathology.Journal of molecular medicine (Berlin, Germany) · 2024Article
- orsai, the Drosophila homolog of human ETFRF1, links lipid catabolism to growth control.BMC biology · 2022Article
- FHL2 anchors mitochondria to actin and adapts mitochondrial dynamics to glucose supply.The Journal of cell biology · 2021Article
- Metabolomics provide new insights into mechanisms of Wolbachia-induced paternal defects in Drosophila melanogaster.PLoS pathogens · 2021Article
- Miro1 Marks Parkinson's Disease Subset and Miro1 Reducer Rescues Neuron Loss in Parkinson's Models.Cell metabolism · 2019Article
- Dendritic Cells Require PINK1-Mediated Phosphorylation of BCKDE1α to Promote Fatty Acid Oxidation for Immune Function.Frontiers in immunology · 2019Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
PTEN-induced putative kinase 1 (PINK1) is a mitochondria-targeted kinase whose mutations are a cause of Parkinson's disease. We set out to better understand PINK1's effects on mitochondrial proteins in vivo. Using an unbiased phosphoproteomic screen in Drosophila, we found that PINK1 mediates the phosphorylation of MCAD, a mitochondrial matrix protein critical to fatty acid metabolism. By mimicking phosphorylation of this protein in a PINK1 null background, we restored PINK1 null's climbing, flight, thorax, and wing deficiencies. Owing to MCAD's role in fatty acid metabolism, we examined the metabolic profile of PINK1 null flies, where we uncovered significant disruptions in both acylcarnitines and amino acids. Some of these disruptions were rescued by phosphorylation of MCAD, consistent with MCAD's rescue of PINK1 null's organismal phenotypes. Our work validates and extends the current knowledge of PINK1, identifies a novel function of MCAD, and illuminates the need for and effectiveness of metabolic profiling in models of neurodegenerative disease.
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