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000164042 0247_ $$2doi$$a10.1016/j.molmet.2022.101503
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000164042 041__ $$aEnglish
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000164042 1001_ $$0P:(DE-2719)2814190$$aJackson, Joshua$$b0$$eFirst author$$udzne
000164042 245__ $$aSGPL1 stimulates VPS39 recruitment to the mitochondria in MICU1 deficient cells.
000164042 260__ $$aOxford [u.a.]$$bElsevier$$c2022
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000164042 520__ $$aMitochondrial '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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000164042 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x1
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000164042 650_7 $$2Other$$aAutophagy
000164042 650_7 $$2Other$$aCaenorhabditis elegans
000164042 650_7 $$2Other$$aLongevity
000164042 650_7 $$2Other$$aMICU1
000164042 650_7 $$2Other$$aMitochondria
000164042 650_7 $$2Other$$aSphingosine signaling
000164042 650_7 $$2Other$$aVPS39
000164042 650_2 $$2MeSH$$aAldehyde-Lyases: metabolism
000164042 650_2 $$2MeSH$$aAnimals
000164042 650_2 $$2MeSH$$aAutophagy-Related Proteins: metabolism
000164042 650_2 $$2MeSH$$aCaenorhabditis elegans
000164042 650_2 $$2MeSH$$aCaenorhabditis elegans Proteins: metabolism
000164042 650_2 $$2MeSH$$aCalcium-Binding Proteins: genetics
000164042 650_2 $$2MeSH$$aCalcium-Binding Proteins: metabolism
000164042 650_2 $$2MeSH$$aMice
000164042 650_2 $$2MeSH$$aMitochondria: metabolism
000164042 650_2 $$2MeSH$$aMitochondrial Membrane Transport Proteins: metabolism
000164042 650_2 $$2MeSH$$aOxidative Phosphorylation
000164042 650_2 $$2MeSH$$aVesicular Transport Proteins: metabolism
000164042 7001_ $$0P:(DE-2719)2811527$$aWischhof, Lena$$b1$$udzne
000164042 7001_ $$0P:(DE-2719)2812562$$aScifo, Enzo$$b2$$udzne
000164042 7001_ $$0P:(DE-2719)9000693$$aPellizzer, Anna$$b3$$udzne
000164042 7001_ $$0P:(DE-2719)9001250$$aWang, Yiru$$b4$$udzne
000164042 7001_ $$0P:(DE-2719)2811171$$aPiazzesi, Antonia$$b5$$udzne
000164042 7001_ $$0P:(DE-2719)9000991$$aGentile, Debora$$b6$$udzne
000164042 7001_ $$0P:(DE-2719)9000992$$aSiddig, Sana$$b7$$udzne
000164042 7001_ $$0P:(DE-2719)2810452$$aStork, Miriam$$b8$$udzne
000164042 7001_ $$aHopkins, Chris E$$b9
000164042 7001_ $$0P:(DE-2719)2812735$$aHändler, Kristian$$b10$$udzne
000164042 7001_ $$aWeis, Joachim$$b11
000164042 7001_ $$aRoos, Andreas$$b12
000164042 7001_ $$0P:(DE-2719)2811660$$aSchultze, Joachim L$$b13$$udzne
000164042 7001_ $$0P:(DE-2719)2010732$$aNicotera, Pierluigi$$b14$$udzne
000164042 7001_ $$0P:(DE-2719)2289209$$aEhninger, Dan$$b15$$udzne
000164042 7001_ $$0P:(DE-2719)2158358$$aBano, Daniele$$b16$$eLast author$$udzne
000164042 773__ $$0PERI:(DE-600)2708735-9$$a10.1016/j.molmet.2022.101503$$gVol. 61, p. 101503 -$$p101503$$tMolecular metabolism$$v61$$x2212-8778$$y2022
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