ArticleMolecular biology of the cell2010
Mitochondrial fragmentation leads to intracellular acidification in Caenorhabditis elegans and mammalian cells.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Lactate-Mediated Brain Acidosis Drives Epigenetic Dysregulation of TGFB2 and Associated Gene Networks in Schizophrenia and Bipolar Disorder.International journal of molecular sciences · 2026Article
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- Kynurenic Acid Protects Against Myocardial Ischemia/Reperfusion Injury by Activating GPR35 Receptors and Preserving Mitochondrial Structure and Function.Biomolecules · 2025Article
- Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels inAntioxidants (Basel, Switzerland) · 2025Review
- Calcineurin-Dependent Homeostatic Response ofCells · 2023Article
- A proton-inhibited DEG/ENaC ion channel maintains neuronal ionstasis and promotes neuronal survival under stress.iScience · 2023Article
- Increased mitochondrial CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Deregulation of Mitochondrial Calcium Handling Due to Presenilin Loss Disrupts Redox Homeostasis and Promotes Neuronal Dysfunction.Antioxidants (Basel, Switzerland) · 2022Article
- Visualizing and quantifying molecular and cellular processes in Caenorhabditis elegans using light microscopy.Genetics · 2022Review
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- Charcot-Marie-tooth disease causing mutation (p.R158H) in pyruvate dehydrogenase kinase 3 (PDK3) affects synaptic transmission, ATP production and causes neurodegeneration in a CMTX6 C. elegans model.Human molecular genetics · 2021Article
- FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.Autophagy · 2021Article
- Ethyl isopropyl amiloride decreases oxidative phosphorylation and increases mitochondrial fusion in clonal untransformed and cancer cells.American journal of physiology. Cell physiology · 2021Article
- In Vivo Imaging with Genetically Encoded Redox Biosensors.International journal of molecular sciences · 2020Review
- Triclosan disrupts immune cell function by depressing CaToxicology and applied pharmacology · 2020Article
- Disruption of mitochondrial dynamics increases stress resistance through activation of multiple stress response pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Autophagy compensates for defects in mitochondrial dynamics.PLoS genetics · 2020Article
- Cell Biology of the Mitochondrion.Genetics · 2017Review
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Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial structural dynamics are regulated through the opposing processes of membrane fission and fusion, which are conserved from yeast to man. The chronic inhibition of mitochondrial fusion as a result of genetic mutation is the cause of human autosomal dominant optic atrophy (ADOA) and Charcot-Marie-Tooth syndrome type 2A (CMT-2A). Here, we demonstrate that genetic fragmentation of the mitochondrial network in Caenorhabditis elegans induces cellular acidification in a broad range of tissues from the intestine, to body wall muscles, and neurons. Genetic epistasis analyses demonstrate that fragmentation itself, and not the loss of a particular protein, leads to acidosis, and the worm's fitness matches the extent of acidification. We suggest that fragmentation may cause acidification through two distinct processes: oxidative signaling after the loss of the ability of the mitochondrial inner membrane to undergo fusion and lactic acidosis after the loss of outer membrane fusion. Finally, experiments in cultured mammalian cells demonstrate a conserved link between mitochondrial morphology and cell pH homeostasis. Taken together these data reveal a potential role for acidosis in the differing etiology of diseases associated with mitochondrial morphology defects such as ADOA and CMT-2A.
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