Home > Publications Database > SGPL1 stimulates VPS39 recruitment to the mitochondria in MICU1 deficient cells. > print

001     164042
005     20230915090545.0
024 7 _ |a pmc:PMC9170783
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024 7 _ |a 10.1016/j.molmet.2022.101503
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037 _ _ |a DZNE-2022-00705
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Jackson, Joshua
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245 _ _ |a SGPL1 stimulates VPS39 recruitment to the mitochondria in MICU1 deficient cells.
260 _ _ |a Oxford [u.a.]
|c 2022
|b Elsevier
336 7 _ |a article
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520 _ _ |a 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.
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650 _ 7 |a Autophagy
|2 Other
650 _ 7 |a Caenorhabditis elegans
|2 Other
650 _ 7 |a Longevity
|2 Other
650 _ 7 |a MICU1
|2 Other
650 _ 7 |a Mitochondria
|2 Other
650 _ 7 |a Sphingosine signaling
|2 Other
650 _ 7 |a VPS39
|2 Other
650 _ 2 |a Aldehyde-Lyases: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Autophagy-Related Proteins: metabolism
|2 MeSH
650 _ 2 |a Caenorhabditis elegans
|2 MeSH
650 _ 2 |a Caenorhabditis elegans Proteins: metabolism
|2 MeSH
650 _ 2 |a Calcium-Binding Proteins: genetics
|2 MeSH
650 _ 2 |a Calcium-Binding Proteins: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mitochondria: metabolism
|2 MeSH
650 _ 2 |a Mitochondrial Membrane Transport Proteins: metabolism
|2 MeSH
650 _ 2 |a Oxidative Phosphorylation
|2 MeSH
650 _ 2 |a Vesicular Transport Proteins: metabolism
|2 MeSH
700 1 _ |a Wischhof, Lena
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700 1 _ |a Scifo, Enzo
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700 1 _ |a Pellizzer, Anna
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700 1 _ |a Wang, Yiru
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700 1 _ |a Piazzesi, Antonia
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700 1 _ |a Gentile, Debora
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700 1 _ |a Siddig, Sana
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700 1 _ |a Stork, Miriam
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700 1 _ |a Hopkins, Chris E
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700 1 _ |a Händler, Kristian
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700 1 _ |a Weis, Joachim
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700 1 _ |a Roos, Andreas
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700 1 _ |a Schultze, Joachim L
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700 1 _ |a Nicotera, Pierluigi
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700 1 _ |a Ehninger, Dan
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700 1 _ |a Bano, Daniele
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773 _ _ |a 10.1016/j.molmet.2022.101503
|g Vol. 61, p. 101503 -
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|t Molecular metabolism
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|x 2212-8778
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