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- W2140155848 abstract "Cells and tissues deficient in mitochondrial fusion have been shown to have defects linked to the exchange of inner membrane (IMM) and matrix components, particularly mitochondrial DNA. Outer membrane (OMM) constituents originate in the cytoplasm, thus the role of intermitochondrial transfer of OMM components by fusion remained unexplored. Here we show that fibroblasts lacking the GTPases responsible for OMM fusion, Mfn1/2, have a more heterogeneous distribution of OMM proteins than wild-type cells, and in particular that heterogeneity of pro-apoptotic Bak leads to dysregulation of Bid-dependent apoptotic signaling. Homogeneous distribution of Bak is partially rescued by introduction of Mfn2 into Mfn1/2-/- cells. Furthermore, fusions between mitochondria lacking and containing Bak result in hybrids sensitive to Bid. Proteins with different modes of OMM association display varying degrees of heterogeneity in Mfn1/2 /- cells and different kinetics of transfer during fusion in fusion-competent cells. Efficient coupling of OMM to IMM fusion depends on the presence of both Mfn isoforms and is antagonized by the mitochondrial fission protein, Drp1. Thus, OMM function depends on mitochondrial fusion and is a locus of dysfunction in conditions of fusion deficiency." @default.
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- W2140155848 date "2013-01-01" @default.
- W2140155848 modified "2023-10-17" @default.
- W2140155848 title "Outer Mitochondrial Membrane Protein Distribution and Function Depend on Mitochondrial Fusion" @default.
- W2140155848 doi "https://doi.org/10.1016/j.bpj.2012.11.3622" @default.
- W2140155848 hasPublicationYear "2013" @default.
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