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@ARTICLE{Hofstadter:614102,
      author       = {Hofstadter, William A. and Cook, Katelyn C. and
                      Tsopurashvili, Elene and Gebauer, Robert and Pražák,
                      Vojtěch and Machala, Emily A. and Park, Ji Woo and
                      Grünewald, Kay and Quemin, Emmanuelle R. J. and Cristea,
                      Ileana M.},
      title        = {{I}nfection-induced peripheral mitochondria fission drives
                      {ER} encapsulations and inter-mitochondria contacts that
                      rescue bioenergetics},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {PUBDB-2024-05736},
      pages        = {7352},
      year         = {2024},
      abstract     = {The dynamic regulation of mitochondria shape via fission
                      and fusion is critical for cellular responses to stimuli. In
                      homeostatic cells, two modes of mitochondrial fission,
                      midzone and peripheral, provide a decision fork between
                      either proliferation or clearance of mitochondria. However,
                      the relationship between specific mitochondria shapes and
                      functions remains unclear in many biological contexts. While
                      commonly associated with decreased bioenergetics, fragmented
                      mitochondria paradoxically exhibit elevated respiration in
                      several disease states, including infection with the
                      prevalent pathogen human cytomegalovirus (HCMV) and
                      metastatic melanoma. Here, incorporating super-resolution
                      microscopy with mass spectrometry and metabolic assays, we
                      use HCMV infection to establish a molecular mechanism for
                      maintaining respiration within a fragmented mitochondria
                      population. We establish that HCMV induces fragmentation
                      through peripheral mitochondrial fission coupled with
                      suppression of mitochondria fusion. Unlike uninfected cells,
                      the progeny of peripheral fission enter mitochondria-ER
                      encapsulations (MENCs) where they are protected from
                      degradation and bioenergetically stabilized during
                      infection. MENCs also stabilize pro-viral inter-mitochondria
                      contacts (IMCs), which electrochemically link mitochondria
                      and promote respiration. Demonstrating a broader relevance,
                      we show that the fragmented mitochondria within metastatic
                      melanoma cells also form MENCs. Our findings establish a
                      mechanism where mitochondria fragmentation can promote
                      increased respiration, a feature relevant in the context of
                      human diseases.},
      cin          = {CSSB-LIV-KG},
      ddc          = {500},
      cid          = {I:(DE-H253)CSSB-LIV-KG-20220525},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      experiment   = {EXP:(DE-MLZ)NOSPEC-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39187492},
      UT           = {WOS:001298967100004},
      doi          = {10.1038/s41467-024-51680-4},
      url          = {https://bib-pubdb1.desy.de/record/614102},
}