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@ARTICLE{Mondal:282567,
      author       = {Mondal, Mrityunjoy and Scifo, Enzo and Ciliberti, Rossella
                      Erminia and Wischhof, Lena and Abbariki, Tannaz Norizadeh
                      and Jackson, Joshua and Menegatou, Ioanna-Maria and
                      Zeisler-Diehl, Viktoria and Riemer, Jan and Jussila,
                      Benjamin and Hopkins, Christopher E and Kierszniowska,
                      Sylwia and Schreiber, Lukas and Nicotera, Pierluigi and
                      Ehninger, Dan and Bano, Daniele},
      title        = {{D}ietary lipid content modifies wah-1/{AIFM}1-associated
                      phenotypes via {LRK}-1 and {DRP}-1 expression in {C}.
                      elegans.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-01330},
      pages        = {10817},
      year         = {2025},
      abstract     = {Eukaryotic cells rely on mitochondria to fine-tune their
                      metabolism in response to environmental and nutritional
                      changes. However, how mitochondria adapt to nutrient
                      availability and how diets impact mitochondrial disease
                      progression, remain unclear. Here, we show that
                      lipid-derived diets influence the survival of Caenorhabditis
                      elegans carrying a hypomorphic wah-1/AIFM1 mutation that
                      compromises mitochondrial Complex I assembly. Comparative
                      proteomic and lipidomic analyses reveal that the overall
                      metabolic profile of wah-1/AIFM1 mutants varies with
                      bacterial diet. Specifically, high-lipid diets extend
                      lifespan by promoting mitochondrial network maintenance and
                      lipid accumulation, whereas low-lipid diets shorten animal
                      survival via overactivation of LRK-1 and DRP-1. We
                      demonstrate that LRK-1 inhibition downregulates DRP-1
                      expression, reduces mitochondrial network fragmentation, and
                      attenuates excessive autophagy, thereby rescuing the
                      survival defects of wah-1 mutants maintained on low-lipid
                      diets. Together, these findings suggest that nutrition, and
                      particularly lipid intake, may ameliorate certain disease
                      phenotypes associated with an inherited mutation that
                      disrupts mitochondrial bioenergetics.},
      keywords     = {Animals / Caenorhabditis elegans: metabolism /
                      Caenorhabditis elegans: genetics / Caenorhabditis elegans
                      Proteins: metabolism / Caenorhabditis elegans Proteins:
                      genetics / Phenotype / Dietary Fats: metabolism / Dietary
                      Fats: pharmacology / Mitochondria: metabolism / Dynamins:
                      metabolism / Dynamins: genetics / Mutation / Longevity /
                      Autophagy / Caenorhabditis elegans Proteins (NLM Chemicals)
                      / Dietary Fats (NLM Chemicals) / Dynamins (NLM Chemicals) /
                      dynamin-related protein 1, C elegans (NLM Chemicals)},
      cin          = {AG Bano / AG Ehninger},
      ddc          = {500},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013005},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41326385},
      doi          = {10.1038/s41467-025-66900-8},
      url          = {https://pub.dzne.de/record/282567},
}