Baker's yeast is a valuable model system for the study of biological aging as it can be utilized for the measurement of replicative and chronological life spans in response to interventions. Whereas replicative aging in Saccharomyces cerevisiae mirrors dividing mammalian cells, chronological aging is seen in non-dividing cells. Aging is strongly influenced by the cellular organelles, especially by mitochondria which house essential functions like oxidative phosphorylation. Additionally, peroxisomes were shown to modulate the aging process, mainly by their turnover of reactive oxygen species. There is a fundamental interest in understanding how mitochondria and peroxisomes contribute to cellular aging. This work analyzes chronological aging in yeast mutants that are affected in peroxisomal proliferation and inheritance. Deletion of INP1 (retention of peroxisomes in the mother cell) or PEX11 (division of peroxisomes) leads to clearly reduced life spans compared to the wild-type control under conditions which depend on peroxisomal metabolism. Δinp1 cells are long-lived in contrast to the wild type and Δpex11 when assayed under conditions that not necessitate peroxisome function. Neither treatment affects the index of respiratory capacity, indicating fully functional mitochondria. Evaluation of stress resistances reveals that Δinp1 has significantly higher resistance to the apoptosis elicitor acetic acid. Old Δpex11 cells from an oleate culture are more susceptible to hydrogen peroxide treatment compared to Δinp1 and the wild type. Finally, aged cells are hyper-sensitive to heat shock treatment in contrast to young cells.

Centro de Investigación y de Estudios Avanzados del IPN Unidad Monterrey Parque de Investigación e Innovación Tecnológica CP 66600 Apodaca Nuevo León Mexico

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EMBO J. 2011 Jan 5;30(1):5-16 PubMed

Biochim Biophys Acta. 2016 May;1863(5):922-33 PubMed

J Cell Biol. 1995 Apr;129(2):345-55 PubMed

Biochim Biophys Acta Biomembr. 2018 Jun;1860(6):1292-1300 PubMed

FEMS Yeast Res. 2016 Jun;16(4): PubMed

J Mol Biol. 2015 Jun 5;427(11):2072-87 PubMed

Biol Open. 2015 Apr 24;4(6):710-21 PubMed

Nat Genet. 1996 Dec;14(4):450-6 PubMed

J Physiol. 2003 Oct 15;552(Pt 2):335-44 PubMed

Yeast. 1998 Jan 30;14(2):115-32 PubMed

Proc Natl Acad Sci U S A. 2015 May 19;112(20):6377-82 PubMed

J Cell Sci. 2018 Feb 7;131(3): PubMed

Subcell Biochem. 2012;57:55-78 PubMed

Cell Cycle. 2015;14(11):1698-703 PubMed

Aging (Albany NY). 2010 Jul;2(7):393-414 PubMed

Biogerontology. 2018 Oct;19(5):303-324 PubMed

FEBS Lett. 2008 Aug 20;582(19):2882-6 PubMed

Arch Microbiol. 1976 Dec 1;111(1-2):137-44 PubMed

Genes Dev. 2007 Oct 1;21(19):2410-21 PubMed

Folia Microbiol (Praha). 2007;52(5):479-83 PubMed

Microsc Res Tech. 2003 Jun 1;61(2):139-50 PubMed

Nature. 2010 Mar 25;464(7288):513-9 PubMed

Traffic. 2011 Mar;12(3):252-9 PubMed

Front Oncol. 2012 May 21;2:50 PubMed

Science. 2014 Jun 20;344(6190):1389-92 PubMed

Dev Cell. 2006 May;10(5):587-600 PubMed

J Cell Biol. 1995 Feb;128(4):509-23 PubMed

Mol Microbiol. 1999 Jul;33(2):274-83 PubMed

J Cell Biol. 2009 Nov 16;187(4):463-71 PubMed

FEBS J. 2009 Mar;276(5):1429-39 PubMed

Proc Natl Acad Sci U S A. 2010 Jul 27;107(30):13348-53 PubMed

Curr Opin Microbiol. 2014 Dec;22:1-7 PubMed

Mol Microbiol. 2017 Jun;104(5):851-868 PubMed

Mol Biol Cell. 2002 Aug;13(8):2598-606 PubMed

J Cell Biol. 2005 Jun 6;169(5):765-75 PubMed

Elife. 2015 Nov 06;4: PubMed

EMBO J. 2013 Sep 11;32(18):2439-53 PubMed