Mitochondria operate as signaling platforms in yeast aging

Medkour, Younes; Titorenko, Vladimir I.

doi:10.18632/aging.100914

Cited by 13 publications

(22 citation statements)

References 7 publications

(15 reference statements)

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“…Of note, our analysis of how different concentrations of LCA impact yeast longevity has revealed that this bile acid delays yeast chronological aging by eliciting a hormetic stress response (Goldberg et al, 2010b; Burstein et al, 2012a), which is characterized by a non-linear and biphasic dose–response curve (Goldberg et al, 2010a; Calabrese and Mattson, 2011; Burstein et al, 2012a; Calabrese et al, 2012; Leonov et al, 2015; Lutchman et al, 2016). Our recent studies also demonstrated that the ability of LCA to elicit such longevity-extending stress response is due in part to alterations in mitochondrial functionality caused by LCA, including changes in the age-related chronology of mitochondrial respiration (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2013, 2015a,b; Arlia-Ciommo et al, 2014a,b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016). These LCA-driven changes in mitochondrial respiration allow mitochondria to establish and sustain an aging-delaying pattern of the entire cell (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2013, 2015a,b; Arlia-Ciommo et al, 2014a,b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016).…”

Section: Resultsmentioning

confidence: 85%

“…Our recent studies also demonstrated that the ability of LCA to elicit such longevity-extending stress response is due in part to alterations in mitochondrial functionality caused by LCA, including changes in the age-related chronology of mitochondrial respiration (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2013, 2015a,b; Arlia-Ciommo et al, 2014a,b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016). These LCA-driven changes in mitochondrial respiration allow mitochondria to establish and sustain an aging-delaying pattern of the entire cell (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2013, 2015a,b; Arlia-Ciommo et al, 2014a,b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016). Enhanced resistance of chronologically aging yeast to chronic oxidative, thermal, and osmotic stresses is part of such LCA-driven cellular pattern (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2015b; Medkour and Titorenko, 2016); this kind of mitochondria-dependent hormetic stress response is called “mitohormesis” (Tapia, 2006; Schulz et al, 2007; Ristow and Zarse, 2010; Ristow, 2014; Yun and Finkel, 2014).…”

Section: Resultsmentioning

confidence: 85%

“…These LCA-driven changes in mitochondrial respiration allow mitochondria to establish and sustain an aging-delaying pattern of the entire cell (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2013, 2015a,b; Arlia-Ciommo et al, 2014a,b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016). Enhanced resistance of chronologically aging yeast to chronic oxidative, thermal, and osmotic stresses is part of such LCA-driven cellular pattern (Goldberg et al, 2010b; Burstein et al, 2012b; Beach et al, 2015b; Medkour and Titorenko, 2016); this kind of mitochondria-dependent hormetic stress response is called “mitohormesis” (Tapia, 2006; Schulz et al, 2007; Ristow and Zarse, 2010; Ristow, 2014; Yun and Finkel, 2014). We thought, therefore, that some of the three long-lived yeast mutants selected under laboratory conditions may have evolved an altered pattern of mitochondrial respiration and/or stress susceptibility.…”

Section: Resultsmentioning

confidence: 99%

“…Several other bile acids can decelerate yeast chronological aging as well, although to a lesser extent than LCA (Goldberg et al, 2010b). We demonstrated that exogenously added LCA enters the yeast cell, accumulates in both mitochondrial membranes, causes a remodeling of mitochondrial membrane lipidome, alters morphology and functionality of mitochondria, and allows mitochondria to establish and sustain an aging-delaying pattern of the entire cell (Burstein et al, 2012b; Beach et al, 2013, 2015b; Burstein and Titorenko, 2014; Medkour and Titorenko, 2016). …”

Section: Introductionmentioning

confidence: 99%

“…Bile acids extend healthy lifespan in animals also because they act as signaling molecules that enable to sustain lipid, glucose, and energy homeostasis (Motola et al, 2006; Gerisch et al, 2007; Russell and Kahn, 2007; Ramalho et al, 2008; Thomas et al, 2008; Amaral et al, 2009; Hylemon et al, 2009; Lefebvre et al, 2009; Monte et al, 2009; Tiwari and Maiti, 2009; Vallim and Edwards, 2009; Goldberg et al, 2011, 2013; Pols et al, 2011; Wollam et al, 2011, 2012; Lee and Schroeder, 2012; Chiang, 2013; de Aguiar Vallim et al, 2013; Groen and Kuipers, 2013; Li and Chiang, 2013; Magner et al, 2013; Arlia-Ciommo et al, 2014b; Mahanti et al, 2014). Moreover, bile acids extend healthy lifespan in animals because these mildly toxic molecules with detergent-like properties can activate detoxification of xenobiotics, thus promoting chemical hormesis and operating as endobiotic regulators of aging that improve health and prolong longevity (Amador-Noguez et al, 2004, 2007; Gems, 2007; Russell and Kahn, 2007; Gems and Partridge, 2008; Burstein et al, 2012a; Arlia-Ciommo et al, 2014b; Li and Chiang, 2014; Medkour and Titorenko, 2016). …”

Section: Introductionmentioning

confidence: 99%

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Empirical Validation of a Hypothesis of the Hormetic Selective Forces Driving the Evolution of Longevity Regulation Mechanisms

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Exogenously added lithocholic bile acid and some other bile acids slow down yeast chronological aging by eliciting a hormetic stress response and altering mitochondrial functionality. Unlike animals, yeast cells do not synthesize bile acids. We therefore hypothesized that bile acids released into an ecosystem by animals may act as interspecies chemical signals that generate selective pressure for the evolution of longevity regulation mechanisms in yeast within this ecosystem. To empirically verify our hypothesis, in this study we carried out a three-step process for the selection of long-lived yeast species by a long-term exposure to exogenous lithocholic bile acid. Such experimental evolution yielded 20 long-lived mutants, three of which were capable of sustaining their considerably prolonged chronological lifespans after numerous passages in medium without lithocholic acid. The extended longevity of each of the three long-lived yeast species was a dominant polygenic trait caused by mutations in more than two nuclear genes. Each of the three mutants displayed considerable alterations to the age-related chronology of mitochondrial respiration and showed enhanced resistance to chronic oxidative, thermal, and osmotic stresses. Our findings empirically validate the hypothesis suggesting that hormetic selective forces can drive the evolution of longevity regulation mechanisms within an ecosystem.

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Mitochondria operate as signaling platforms in yeast aging

Cited by 13 publications

References 7 publications

Empirical Validation of a Hypothesis of the Hormetic Selective Forces Driving the Evolution of Longevity Regulation Mechanisms

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