Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells

Besides their role as a storage for neutral lipids and sterols, there is increasing evidence that lipid droplets (LDs) are involved in cellular detoxification. LDs are in close contact to a broad variety of organelles where protein- and lipid exchange is mediated. Mitochondria as a main driver of th...

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Autores principales: Melanie Kovacs, Florian Geltinger, Thomas Verwanger, Richard Weiss, Klaus Richter, Mark Rinnerthaler
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Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/897c29ae2fc6443d895dcf706d2318fb
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spelling oai:doaj.org-article:897c29ae2fc6443d895dcf706d2318fb2021-11-19T05:49:44ZLipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells2296-634X10.3389/fcell.2021.774985https://doaj.org/article/897c29ae2fc6443d895dcf706d2318fb2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.774985/fullhttps://doaj.org/toc/2296-634XBesides their role as a storage for neutral lipids and sterols, there is increasing evidence that lipid droplets (LDs) are involved in cellular detoxification. LDs are in close contact to a broad variety of organelles where protein- and lipid exchange is mediated. Mitochondria as a main driver of the aging process produce reactive oxygen species (ROS), which damage several cellular components. LDs as highly dynamic organelles mediate a potent detoxification mechanism by taking up toxic lipids and proteins. A stimulation of LDs induced by the simultaneously overexpression of Lro1p and Dga1p (both encoding acyltransferases) prolongs the chronological as well as the replicative lifespan of yeast cells. The increased number of LDs reduces mitochondrial fragmentation as well as mitochondrial ROS production, both phenotypes that are signs of aging. Strains with an altered LD content or morphology as in the sei1∆ or lro1∆ mutant lead to a reduced replicative lifespan. In a yeast strain defective for the LON protease Pim1p, which showed an enhanced ROS production, increased doubling time and an altered mitochondrial morphology, a LRO1 overexpression resulted in a partially reversion of this “premature aging” phenotype.Melanie KovacsFlorian GeltingerThomas VerwangerRichard WeissKlaus RichterMark RinnerthalerFrontiers Media S.A.articleaginglipid droplet (LD)protein homeostaismitochondrial damageROS-reactive oxygen speciesBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution DOAJ
collection DOAJ
language EN
topic aging
lipid droplet (LD)
protein homeostais
mitochondrial damage
ROS-
reactive oxygen species
Biology (General)
QH301-705.5
spellingShingle aging
lipid droplet (LD)
protein homeostais
mitochondrial damage
ROS-
reactive oxygen species
Biology (General)
QH301-705.5
Melanie Kovacs
Florian Geltinger
Thomas Verwanger
Richard Weiss
Klaus Richter
Mark Rinnerthaler
Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
description Besides their role as a storage for neutral lipids and sterols, there is increasing evidence that lipid droplets (LDs) are involved in cellular detoxification. LDs are in close contact to a broad variety of organelles where protein- and lipid exchange is mediated. Mitochondria as a main driver of the aging process produce reactive oxygen species (ROS), which damage several cellular components. LDs as highly dynamic organelles mediate a potent detoxification mechanism by taking up toxic lipids and proteins. A stimulation of LDs induced by the simultaneously overexpression of Lro1p and Dga1p (both encoding acyltransferases) prolongs the chronological as well as the replicative lifespan of yeast cells. The increased number of LDs reduces mitochondrial fragmentation as well as mitochondrial ROS production, both phenotypes that are signs of aging. Strains with an altered LD content or morphology as in the sei1∆ or lro1∆ mutant lead to a reduced replicative lifespan. In a yeast strain defective for the LON protease Pim1p, which showed an enhanced ROS production, increased doubling time and an altered mitochondrial morphology, a LRO1 overexpression resulted in a partially reversion of this “premature aging” phenotype.
format article
author Melanie Kovacs
Florian Geltinger
Thomas Verwanger
Richard Weiss
Klaus Richter
Mark Rinnerthaler
author_facet Melanie Kovacs
Florian Geltinger
Thomas Verwanger
Richard Weiss
Klaus Richter
Mark Rinnerthaler
author_sort Melanie Kovacs
title Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
title_short Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
title_full Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
title_fullStr Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
title_full_unstemmed Lipid Droplets Protect Aging Mitochondria and Thus Promote Lifespan in Yeast Cells
title_sort lipid droplets protect aging mitochondria and thus promote lifespan in yeast cells
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/897c29ae2fc6443d895dcf706d2318fb
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AT thomasverwanger lipiddropletsprotectagingmitochondriaandthuspromotelifespaninyeastcells
AT richardweiss lipiddropletsprotectagingmitochondriaandthuspromotelifespaninyeastcells
AT klausrichter lipiddropletsprotectagingmitochondriaandthuspromotelifespaninyeastcells
AT markrinnerthaler lipiddropletsprotectagingmitochondriaandthuspromotelifespaninyeastcells
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