scholarly journals Caloric restriction creates a metabolic pattern of chronological aging delay that in budding yeast differs from the metabolic design established by two other geroprotectors

Oncotarget ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 608-625
Author(s):  
Karamat Mohammad ◽  
Vladimir I. Titorenko
Keyword(s):  
Caloric Restriction ◽  
Budding Yeast ◽  
Metabolic Pattern ◽  
Chronological Aging ◽  
Metabolic Design

scholarly journals Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast

2020 ◽  
Vol 21 (13) ◽  
pp. 4717
Author(s):  
Karamat Mohammad ◽  
Jennifer Anne Baratang Junio ◽  
Tala Tafakori ◽  
Emmanuel Orfanos ◽  
Vladimir I. Titorenko
Keyword(s):  
Caloric Restriction ◽  
Budding Yeast ◽  
Yeast Cells ◽  
Yeast Culture ◽  
Chronological Aging ◽  
Quiescent Cells ◽  
Cellular Events ◽  
Age Related ◽  
Calorie Diet ◽  
Cellular Quiescence

After Saccharomyces cerevisiae cells cultured in a medium with glucose consume glucose, the sub-populations of quiescent and non-quiescent cells develop in the budding yeast culture. An age-related chronology of quiescent and non-quiescent yeast cells within this culture is discussed here. We also describe various hallmarks of quiescent and non-quiescent yeast cells. A complex aging-associated program underlies cellular quiescence in budding yeast. This quiescence program includes a cascade of consecutive cellular events orchestrated by an intricate signaling network. We examine here how caloric restriction, a low-calorie diet that extends lifespan and healthspan in yeast and other eukaryotes, influences the cellular quiescence program in S. cerevisiae. One of the main objectives of this review is to stimulate an exploration of the mechanisms that link cellular quiescence to chronological aging of budding yeast. Yeast chronological aging is defined by the length of time during which a yeast cell remains viable after its growth and division are arrested, and it becomes quiescent. We propose a hypothesis on how caloric restriction can slow chronological aging of S. cerevisiae by altering the chronology and properties of quiescent cells. Our hypothesis posits that caloric restriction delays yeast chronological aging by targeting four different processes within quiescent cells.

scholarly journals Growth signaling promotes chronological aging in budding yeast by inducing superoxide anions that inhibit quiescence

Aging ◽  
2010 ◽  
Vol 2 (10) ◽  
pp. 709-726 ◽  
Author(s):  
Martin Weinberger ◽  
Ana Mesquita ◽  
Timothy Carroll ◽  
Laura Marks ◽  
Hui Yang ◽  
...  
Keyword(s):  
Budding Yeast ◽  
Superoxide Anions ◽  
Chronological Aging

scholarly journals In S. cerevisiae hydroxycitric acid antagonizes chronological aging and apoptosis regardless of citrate lyase

APOPTOSIS ◽  
2020 ◽  
Vol 25 (9-10) ◽  
pp. 686-696
Author(s):  
Maurizio D. Baroni ◽  
Sonia Colombo ◽  
Olivier Libens ◽  
Rani Pallavi ◽  
Marco Giorgio ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Mechanistic Model ◽  
Yeast Cells ◽  
Signal Pathways ◽  
Atp Citrate Lyase ◽  
Chronological Aging ◽  
Hydroxycitric Acid ◽  
Age Related ◽  
Citrate Lyase ◽  
Bona Fide

Abstract Caloric restriction mimetics (CRMs) are promising molecules to prevent age-related diseases as they activate pathways driven by a true caloric restriction. Hydroxycitric acid (HCA) is considered a bona fide CRM since it depletes acetyl-CoA pools by acting as a competitive inhibitor of ATP citrate lyase (ACLY), ultimately repressing protein acetylation and promoting autophagy. Importantly, it can reduce inflammation and tumour development. In order to identify phenotypically relevant new HCA targets we have investigated HCA effects in Saccharomyces cerevisiae, where ACLY is lacking. Strikingly, the drug revealed a powerful anti-aging effect, another property proposed to mark bona fide CRMs. Chronological life span (CLS) extension but also resistance to acetic acid of HCA treated cells were associated to repression of cell apoptosis and necrosis. HCA also largely prevented cell deaths caused by a severe oxidative stress. The molecule could act widely by negatively modulating cell metabolism, similarly to citrate. Indeed, it inhibited both growth reactivation and the oxygen consumption rate of yeast cells in stationary phase. Genetic analyses on yeast CLS mutants indicated that part of the HCA effects can be sensed by Sch9 and Ras2, two conserved key regulators of nutritional and stress signal pathways of primary importance. Our data together with published biochemical analyses indicate that HCA may act with multiple mechanisms together with ACLY repression and allowed us to propose an integrated mechanistic model as a basis for future investigations.

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