ArticleMolecular biology of the cell2025
Alterations in lipid saturation trigger remodeling of the outer mitochondrial membrane.
Article in Molecular biology of the cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Mitochondrial-derived compartments buffer outer membrane protein load during acute mitochondrial adaptation.bioRxiv : the preprint server for biology · 2026Article
- Organelle-specific lipid profiles influence/underlie metabolic health in a nutrition-dependent manner.bioRxiv : the preprint server for biology · 2025Article
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8 authors.
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Abstract
Lipid saturation is a key determinant of membrane function and organelle health, with changes in saturation triggering adaptive quality control mechanisms to maintain membrane integrity. Among cellular membranes, the outer mitochondrial membrane (OMM) is an important interface for many cellular functions, but how lipid saturation impacts OMM function remains unclear. Here, we show that increased intracellular unsaturated fatty acids (UFA) remodel the OMM by promoting the formation of multilamellar mitochondrial-derived compartments (MDC), which sequester proteins and lipids from the OMM. These effects depend on the incorporation of UFAs into membrane phospholipids, suggesting that changes in membrane bilayer composition mediate this process. Furthermore, elevated UFAs impair the assembly of the OMM protein translocase (TOM, translocase of the outer membrane) complex, with unassembled TOM components captured into MDCs. Collectively, these findings suggest that alterations in phospholipid saturation may destabilize OMM protein complexes and trigger an adaptive response to sequester excess membrane proteins through MDC formation.
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