ArticlePLoS genetics2020
PE homeostasis rebalanced through mitochondria-ER lipid exchange prevents retinal degeneration in Drosophila.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Implications of mitochondrial phosphatidylethanolamine in neuronal health and neurodegeneration.Neural regeneration research · 2026Article
- Identification of regulatory candidate genes for Lentinula edodes pileus development based on transcriptome analysis.G3 (Bethesda, Md.) · 2026Article
- SMAC/DIABLO: A Guardian Angel in Boosting Anticancer Drug-Induced Apoptosis.Current molecular medicine · 2026Review
- Age-associated reduction in ER-Mitochondrial contacts impairs mitochondrial lipid metabolism and autophagosome formation in the heart.Cell death and differentiation · 2025Article
- Phospholipid biogenesis maintains neuronal integrity during aging and axon regeneration.Genetics · 2025Article
- Organ-resolved lipid mapping inFrontiers in chemistry · 2025Article
- SLMO transfers phosphatidylserine between the outer and inner mitochondrial membrane in Drosophila.PLoS biology · 2024Article
- Exploring the Wilderness within: An Integrative Metabolomics and Transcriptomics Study on Near-Wild and ColonizedInsects · 2024Article
- Mitochondria-associated endoplasmic reticulum membranes as a therapeutic target for cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Metabolomics study of APETx2 post-conditioning on myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2024Article
- PERK prevents rhodopsin degradation during retinitis pigmentosa by inhibiting IRE1-induced autophagy.The Journal of cell biology · 2023Article
- Article
- ER-mitochondria contact sites; a multifaceted factory for CaFrontiers in cell and developmental biology · 2022Review
- Mitochondria-associated endoplasmic reticulum membranes and cardiac hypertrophy: Molecular mechanisms and therapeutic targets.Frontiers in cardiovascular medicine · 2022Review
- Phosphatidylethanolamine homeostasis under conditions of impaired CDP-ethanolamine pathway or phosphatidylserine decarboxylation.Frontiers in nutrition · 2022Review
- Protective Mechanism of Gandou Decoction in a Copper-Laden Hepatolenticular Degeneration Model:Frontiers in pharmacology · 2022Article
- Application of Fluorescent Proteins for Functional Dissection of theInternational journal of molecular sciences · 2021Review
- Structure and Function of Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Role in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2021Review
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major glycerophospholipid phosphatidylethanolamine (PE) in the nervous system is essential for neural development and function. There are two major PE synthesis pathways, the CDP-ethanolamine pathway in the endoplasmic reticulum (ER) and the phosphatidylserine decarboxylase (PSD) pathway in mitochondria. However, the role played by mitochondrial PE synthesis in maintaining cellular PE homeostasis is unknown. Here, we show that Drosophila pect (phosphoethanolamine cytidylyltransferase) mutants lacking the CDP-ethanolamine pathway, exhibited alterations in phospholipid composition, defective phototransduction, and retinal degeneration. Induction of the PSD pathway fully restored levels and composition of cellular PE, thus rescued the retinal degeneration and defective visual responses in pect mutants. Disrupting lipid exchange between mitochondria and ER blocked the ability of PSD to rescue pect mutant phenotypes. These findings provide direct evidence that the synthesis of PE in mitochondria contributes to cellular PE homeostasis, and suggest the induction of mitochondrial PE synthesis as a promising therapeutic approach for disorders associated with PE deficiency.
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