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@ARTICLE{Jackson:164042,
      author       = {Jackson, Joshua and Wischhof, Lena and Scifo, Enzo and
                      Pellizzer, Anna and Wang, Yiru and Piazzesi, Antonia and
                      Gentile, Debora and Siddig, Sana and Stork, Miriam and
                      Hopkins, Chris E and Händler, Kristian and Weis, Joachim
                      and Roos, Andreas and Schultze, Joachim L and Nicotera,
                      Pierluigi and Ehninger, Dan and Bano, Daniele},
      title        = {{SGPL}1 stimulates {VPS}39 recruitment to the mitochondria
                      in {MICU}1 deficient cells.},
      journal      = {Molecular metabolism},
      volume       = {61},
      issn         = {2212-8778},
      address      = {Oxford [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2022-00705},
      pages        = {101503},
      year         = {2022},
      abstract     = {Mitochondrial 'retrograde' signaling may stimulate
                      organelle biogenesis as a compensatory adaptation to
                      aberrant activity of the oxidative phosphorylation (OXPHOS)
                      system. To maintain energy-consuming processes in OXPHOS
                      deficient cells, alternative metabolic pathways are
                      functionally coupled to the degradation, recycling and
                      redistribution of biomolecules across distinct intracellular
                      compartments. While transcriptional regulation of
                      mitochondrial network expansion has been the focus of many
                      studies, the molecular mechanisms promoting mitochondrial
                      maintenance in energy-deprived cells remain poorly
                      investigated.We performed transcriptomics, quantitative
                      proteomics and lifespan assays to identify pathways that are
                      mechanistically linked to mitochondrial network expansion
                      and homeostasis in Caenorhabditis elegans lacking the
                      mitochondrial calcium uptake protein 1 (MICU-1/MICU1). To
                      support our findings, we carried out biochemical and image
                      analyses in mammalian cells and mouse-derived tissues.We
                      report that micu-1(null) mutations impair the OXPHOS system
                      and promote C. elegans longevity through a transcriptional
                      program that is independent of the mitochondrial calcium
                      uniporter MCU-1/MCU and the essential MCU regulator
                      EMRE-1/EMRE. We identify sphingosine phosphate lyase
                      SPL-1/SGPL1 and the ATFS-1-target HOPS complex subunit
                      VPS-39/VPS39 as critical lifespan modulators of micu-1(null)
                      mutant animals. Cross-species investigation indicates that
                      SGPL1 upregulation stimulates VPS39 recruitment to the
                      mitochondria, thereby enhancing mitochondria-lysosome
                      contacts. Consistently, VPS39 downregulation compromises
                      mitochondrial network maintenance and basal autophagic flux
                      in MICU1 deficient cells. In mouse-derived muscles, we show
                      that VPS39 recruitment to the mitochondria may represent a
                      common signature associated with altered OXPHOS system.Our
                      findings reveal a previously unrecognized SGPL1/VPS39 axis
                      that stimulates intracellular organelle interactions and
                      sustains autophagy and mitochondrial homeostasis in OXPHOS
                      deficient cells.},
      keywords     = {Aldehyde-Lyases: metabolism / Animals / Autophagy-Related
                      Proteins: metabolism / Caenorhabditis elegans /
                      Caenorhabditis elegans Proteins: metabolism /
                      Calcium-Binding Proteins: genetics / Calcium-Binding
                      Proteins: metabolism / Mice / Mitochondria: metabolism /
                      Mitochondrial Membrane Transport Proteins: metabolism /
                      Oxidative Phosphorylation / Vesicular Transport Proteins:
                      metabolism / Autophagy (Other) / Caenorhabditis elegans
                      (Other) / Longevity (Other) / MICU1 (Other) / Mitochondria
                      (Other) / Sphingosine signaling (Other) / VPS39 (Other)},
      cin          = {AG Bano / AG Ehninger / AG Schultze / $R\&D$ PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013005 /
                      I:(DE-2719)1013031 / I:(DE-2719)5000031},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9170783},
      pubmed       = {pmid:35452878},
      doi          = {10.1016/j.molmet.2022.101503},
      url          = {https://pub.dzne.de/record/164042},
}