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Communications between Mitochondria, the Nucleus, Vacuoles, Peroxisomes, the Endoplasmic Reticulum, the Plasma Membrane, Lipid Droplets, and the Cytosol during Yeast Chronological Aging

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ABSTRACT

Studies employing the budding yeast Saccharomyces cerevisiae as a model organism have provided deep insights into molecular mechanisms of cellular and organismal aging in multicellular eukaryotes and have demonstrated that the main features of biological aging are evolutionarily conserved. Aging in S. cerevisiae is studied by measuring replicative or chronological lifespan. Yeast replicative aging is likely to model aging of mitotically competent human cell types, while yeast chronological aging is believed to mimic aging of post-mitotic human cell types. Emergent evidence implies that various organelle-organelle and organelle-cytosol communications play essential roles in chronological aging of S. cerevisiae. The molecular mechanisms underlying the vital roles of intercompartmental communications in yeast chronological aging have begun to emerge. The scope of this review is to critically analyze recent progress in understanding such mechanisms. Our analysis suggests a model for how temporally and spatially coordinated movements of certain metabolites between various cellular compartments impact yeast chronological aging. In our model, diverse changes in these key metabolites are restricted to critical longevity-defining periods of chronological lifespan. In each of these periods, a limited set of proteins responds to such changes of the metabolites by altering the rate and efficiency of a certain cellular process essential for longevity regulation. Spatiotemporal dynamics of alterations in these longevity-defining cellular processes orchestrates the development and maintenance of a pro- or anti-aging cellular pattern.

No MeSH data available.


A model for how various organelle-organelle and organelle-cytosol communications impact yeast chronological aging. These communications involve movements of certain metabolites between various cellular compartments. Different changes in these metabolites are temporally restricted to longevity-defining periods called checkpoints. At each checkpoint, the changes of these metabolites are detected by certain master regulator proteins. Because each of the master regulator proteins modulates certain longevity-defining cellular processes, a coordinated in space and time action of these proteins orchestrates the development and maintenance of a pro- or anti-aging cellular pattern. See text for details. Ac-Carnitine, acetyl-carnitine; Ac-CoA, acetyl-CoA; AcOH, acetic acid; DAG, diacylglycerol; EtOH, ethanol; FFA, free (non-esterified) fatty acids; m5c-tRNAs, 5-methylcytosine tRNAs; PKA, protein kinase A; PM, the plasma membrane; ROS, reactive oxygen species; TAG, triacylglycerols; TCA, tricarboxylic; TORC, target of rapamycin complex; tRNAs, transfer RNAs.
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Figure 1: A model for how various organelle-organelle and organelle-cytosol communications impact yeast chronological aging. These communications involve movements of certain metabolites between various cellular compartments. Different changes in these metabolites are temporally restricted to longevity-defining periods called checkpoints. At each checkpoint, the changes of these metabolites are detected by certain master regulator proteins. Because each of the master regulator proteins modulates certain longevity-defining cellular processes, a coordinated in space and time action of these proteins orchestrates the development and maintenance of a pro- or anti-aging cellular pattern. See text for details. Ac-Carnitine, acetyl-carnitine; Ac-CoA, acetyl-CoA; AcOH, acetic acid; DAG, diacylglycerol; EtOH, ethanol; FFA, free (non-esterified) fatty acids; m5c-tRNAs, 5-methylcytosine tRNAs; PKA, protein kinase A; PM, the plasma membrane; ROS, reactive oxygen species; TAG, triacylglycerols; TCA, tricarboxylic; TORC, target of rapamycin complex; tRNAs, transfer RNAs.

Mentions: Recent studies have revealed that various intercompartmental communications (i.e., organelle-organelle and organelle-cytosol) play essential roles in chronological aging of yeast cultured in media with glucose as the only carbon source (Beach and Titorenko, 2011; Beach et al., 2012, 2015a; Leonov and Titorenko, 2013; Medkour and Titorenko, 2016b). A model for how such communications impact yeast chronological aging is depicted schematically in Figure 1. Our model includes the notion that the longevity-defining intercompartmental communications involve unidirectional and bidirectional movements of a distinct set of metabolites between mitochondria and the cytosol, mitochondria and peroxisomes, mitochondria and the nucleus, peroxisomes and the nucleus, mitochondria and vacuoles, the endoplasmic reticulum (ER) and the plasma membrane (PM), the ER and the cytosol, the PM and the cytosol, the PM and vacuoles, the ER and lipid droplets (LD), and LD and peroxisomes (Figure 1). The intracellular concentrations of such metabolites and/or the rates of their movement between cellular compartments undergo age-related changes. In our model, different changes of the key metabolites are temporally restricted to several longevity-defining periods; the term “checkpoints” has been coined to describe these critical periods in yeast chronological lifespan (Burstein et al., 2012; Kyryakov et al., 2012; Arlia-Ciommo et al., 2014a; Beach et al., 2015a,b) (Figure 1). Most of these checkpoints occur early in life of chronologically aging yeast cells, during diauxic (D), and post-diauxic (PD) growth phases. Some of the checkpoints are late-life checkpoints that exists in the non-proliferative stationary (ST) phase of culturing. At each of these checkpoints, the changes of the key metabolites are detected by a distinct set of checkpoint-specific proteins called “master regulators” (Arlia-Ciommo et al., 2014a; Beach et al., 2015a). Our model further posits that each of these master regulators can respond to a change of the detected key metabolite by altering the rate and efficiency of a certain cellular process essential for longevity regulation (Figure 1). By establishing the rates and efficiencies of different longevity-defining cellular processes throughout chronological lifespan, the checkpoint-specific master regulators set up a pro- or anti-aging cellular pattern (Arlia-Ciommo et al., 2014a; Beach et al., 2015a).


Communications between Mitochondria, the Nucleus, Vacuoles, Peroxisomes, the Endoplasmic Reticulum, the Plasma Membrane, Lipid Droplets, and the Cytosol during Yeast Chronological Aging
A model for how various organelle-organelle and organelle-cytosol communications impact yeast chronological aging. These communications involve movements of certain metabolites between various cellular compartments. Different changes in these metabolites are temporally restricted to longevity-defining periods called checkpoints. At each checkpoint, the changes of these metabolites are detected by certain master regulator proteins. Because each of the master regulator proteins modulates certain longevity-defining cellular processes, a coordinated in space and time action of these proteins orchestrates the development and maintenance of a pro- or anti-aging cellular pattern. See text for details. Ac-Carnitine, acetyl-carnitine; Ac-CoA, acetyl-CoA; AcOH, acetic acid; DAG, diacylglycerol; EtOH, ethanol; FFA, free (non-esterified) fatty acids; m5c-tRNAs, 5-methylcytosine tRNAs; PKA, protein kinase A; PM, the plasma membrane; ROS, reactive oxygen species; TAG, triacylglycerols; TCA, tricarboxylic; TORC, target of rapamycin complex; tRNAs, transfer RNAs.
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Figure 1: A model for how various organelle-organelle and organelle-cytosol communications impact yeast chronological aging. These communications involve movements of certain metabolites between various cellular compartments. Different changes in these metabolites are temporally restricted to longevity-defining periods called checkpoints. At each checkpoint, the changes of these metabolites are detected by certain master regulator proteins. Because each of the master regulator proteins modulates certain longevity-defining cellular processes, a coordinated in space and time action of these proteins orchestrates the development and maintenance of a pro- or anti-aging cellular pattern. See text for details. Ac-Carnitine, acetyl-carnitine; Ac-CoA, acetyl-CoA; AcOH, acetic acid; DAG, diacylglycerol; EtOH, ethanol; FFA, free (non-esterified) fatty acids; m5c-tRNAs, 5-methylcytosine tRNAs; PKA, protein kinase A; PM, the plasma membrane; ROS, reactive oxygen species; TAG, triacylglycerols; TCA, tricarboxylic; TORC, target of rapamycin complex; tRNAs, transfer RNAs.
Mentions: Recent studies have revealed that various intercompartmental communications (i.e., organelle-organelle and organelle-cytosol) play essential roles in chronological aging of yeast cultured in media with glucose as the only carbon source (Beach and Titorenko, 2011; Beach et al., 2012, 2015a; Leonov and Titorenko, 2013; Medkour and Titorenko, 2016b). A model for how such communications impact yeast chronological aging is depicted schematically in Figure 1. Our model includes the notion that the longevity-defining intercompartmental communications involve unidirectional and bidirectional movements of a distinct set of metabolites between mitochondria and the cytosol, mitochondria and peroxisomes, mitochondria and the nucleus, peroxisomes and the nucleus, mitochondria and vacuoles, the endoplasmic reticulum (ER) and the plasma membrane (PM), the ER and the cytosol, the PM and the cytosol, the PM and vacuoles, the ER and lipid droplets (LD), and LD and peroxisomes (Figure 1). The intracellular concentrations of such metabolites and/or the rates of their movement between cellular compartments undergo age-related changes. In our model, different changes of the key metabolites are temporally restricted to several longevity-defining periods; the term “checkpoints” has been coined to describe these critical periods in yeast chronological lifespan (Burstein et al., 2012; Kyryakov et al., 2012; Arlia-Ciommo et al., 2014a; Beach et al., 2015a,b) (Figure 1). Most of these checkpoints occur early in life of chronologically aging yeast cells, during diauxic (D), and post-diauxic (PD) growth phases. Some of the checkpoints are late-life checkpoints that exists in the non-proliferative stationary (ST) phase of culturing. At each of these checkpoints, the changes of the key metabolites are detected by a distinct set of checkpoint-specific proteins called “master regulators” (Arlia-Ciommo et al., 2014a; Beach et al., 2015a). Our model further posits that each of these master regulators can respond to a change of the detected key metabolite by altering the rate and efficiency of a certain cellular process essential for longevity regulation (Figure 1). By establishing the rates and efficiencies of different longevity-defining cellular processes throughout chronological lifespan, the checkpoint-specific master regulators set up a pro- or anti-aging cellular pattern (Arlia-Ciommo et al., 2014a; Beach et al., 2015a).

View Article: PubMed Central - PubMed

ABSTRACT

Studies employing the budding yeast Saccharomyces cerevisiae as a model organism have provided deep insights into molecular mechanisms of cellular and organismal aging in multicellular eukaryotes and have demonstrated that the main features of biological aging are evolutionarily conserved. Aging in S. cerevisiae is studied by measuring replicative or chronological lifespan. Yeast replicative aging is likely to model aging of mitotically competent human cell types, while yeast chronological aging is believed to mimic aging of post-mitotic human cell types. Emergent evidence implies that various organelle-organelle and organelle-cytosol communications play essential roles in chronological aging of S. cerevisiae. The molecular mechanisms underlying the vital roles of intercompartmental communications in yeast chronological aging have begun to emerge. The scope of this review is to critically analyze recent progress in understanding such mechanisms. Our analysis suggests a model for how temporally and spatially coordinated movements of certain metabolites between various cellular compartments impact yeast chronological aging. In our model, diverse changes in these key metabolites are restricted to critical longevity-defining periods of chronological lifespan. In each of these periods, a limited set of proteins responds to such changes of the metabolites by altering the rate and efficiency of a certain cellular process essential for longevity regulation. Spatiotemporal dynamics of alterations in these longevity-defining cellular processes orchestrates the development and maintenance of a pro- or anti-aging cellular pattern.

No MeSH data available.