Research Papers:

Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death

Anthony Arlia-Ciommo, Anna Leonov, Adam Beach, Vincent R. Richard, Simon D. Bourque, Michelle T. Burstein, Pavlo Kyryakov, Alejandra Gomez-Perez, Olivia Koupaki, Rachel Feldman and Vladimir I. Titorenko _

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Oncotarget. 2018; 9:16163-16184. https://doi.org/10.18632/oncotarget.24604

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Anthony Arlia-Ciommo1, Anna Leonov1, Adam Beach1, Vincent R. Richard1, Simon D. Bourque1, Michelle T. Burstein1, Pavlo Kyryakov1, Alejandra Gomez-Perez1, Olivia Koupaki1, Rachel Feldman1 and Vladimir I. Titorenko1

1Department of Biology, Concordia University, Montreal, Quebec, Canada

Correspondence to:

Vladimir I. Titorenko, email: [email protected]

Keywords: yeast; cellular aging; caloric restriction; metabolism; mitochondria

Received: November 03, 2017     Accepted: February 25, 2018     Epub: March 05, 2018      Published: March 23, 2018


A dietary regimen of caloric restriction delays aging in evolutionarily distant eukaryotes, including the budding yeast Saccharomyces cerevisiae. Here, we assessed how caloric restriction influences morphological, biochemical and cell biological properties of chronologically aging yeast advancing through different stages of the aging process. Our findings revealed that this low-calorie diet slows yeast chronological aging by mechanisms that coordinate the spatiotemporal dynamics of various cellular processes before entry into a non-proliferative state and after such entry. Caloric restriction causes a stepwise establishment of an aging-delaying cellular pattern by tuning a network that assimilates the following: 1) pathways of carbohydrate and lipid metabolism; 2) communications between the endoplasmic reticulum, lipid droplets, peroxisomes, mitochondria and the cytosol; and 3) a balance between the processes of mitochondrial fusion and fission. Through different phases of the aging process, the caloric restriction-dependent remodeling of this intricate network 1) postpones the age-related onsets of apoptotic and liponecrotic modes of regulated cell death; and 2) actively increases the chance of cell survival by supporting the maintenance of cellular proteostasis. Because caloric restriction decreases the risk of cell death and actively increases the chance of cell survival throughout chronological lifespan, this dietary intervention extends longevity of chronologically aging yeast.

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