Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast

Mohammad, Karamat; Junio, Jennifer Anne Baratang; Tafakori, Tala; Orfanos, Emmanuel; Titorenko, Vladimir I.

doi:10.3390/ijms21134717

Cited by 14 publications

(20 citation statements)

References 112 publications

(310 reference statements)

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“…For example, null mutations in quiescence‐regulating genes including TOR1 and SCH9 (a major target of TOR1) are reported to extend the CLS of yeast cells (Fabrizio, Pozza, Pletcher, Gendron, & Longo, 2001; Paola Fabrizio & Longo, 2003; Powers, Kaeberlein, Caldwell, Kennedy, & Fields, 2006; Wei et al, 2008). Mechanisms linking chronological aging to cellular quiescence in budding yeast in response to carbon starvation have been discussed in a recent review (Mohammad , Baratang Junio, Tafakori, Orfanos, & Titorenko, 2020).…”

Section: Introductionmentioning

confidence: 99%

Cellular quiescence in budding yeast

Sun

Gresham

2021

Yeast

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Cellular quiescence, the temporary and reversible exit from proliferative growth, is the predominant state of all cells. However, our understanding of the biological processes and molecular mechanisms that underlie cell quiescence remains incomplete. As with the mitotic cell cycle, budding and fission yeast are preeminent model systems for studying cellular quiescence owing to their rich experimental toolboxes and the evolutionary conservation across eukaryotes of pathways and processes that control quiescence. Here, we review current knowledge of cell quiescence in budding yeast and how it pertains to cellular quiescence in other organisms, including multicellular animals. Quiescence entails large‐scale remodeling of virtually every cellular process, organelle, gene expression, and metabolic state that is executed dynamically as cells undergo the initiation, maintenance, and exit from quiescence. We review these major transitions, our current understanding of their molecular bases, and highlight unresolved questions. We summarize the primary methods employed for quiescence studies in yeast and discuss their relative merits. Understanding cell quiescence has important consequences for human disease as quiescent single‐celled microbes are notoriously difficult to kill and quiescent human cells play important roles in diseases such as cancer. We argue that research on cellular quiescence will be accelerated through the adoption of common criteria, and methods, for defining cell quiescence. An integrated approach to studying cell quiescence, and a focus on the behavior of individual cells, will yield new insights into the pathways and processes that underlie cell quiescence leading to a more complete understanding of the life cycle of cells. Take Away Quiescent cells are viable cells that have reversibly exited the cell cycle Quiescence is induced in response to a variety of nutrient starvation signals Quiescence is executed dynamically through three phases: initiation, maintenance, and exit Quiescence entails large‐scale remodeling of gene expression, organelles, and metabolism Single‐cell approaches are required to address heterogeneity among quiescent cells

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Section: Introductionmentioning

confidence: 99%

Cellular quiescence in budding yeast

Sun

Gresham

2021

Yeast

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“…This gives possibilities to follow the overall metabolic switch during the lifespan and study certain factors that control this. Recently there has been a huge amount of research on yeast CLS aimed at using these unicellular eukaryotes as a model for testing the antiaging activities of different compounds [ 12 , 13 ] and for studying the fine molecular mechanisms that underlie the process, including research on cellular metabolism and telomere biology in regard to aging [ 14 , 15 ]. Moreover, personal perspectives also appeared highlighting the importance of the yeast CLS research as a compelling stipulation for providing really deep insights on the process in higher eukaryotes [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Changes in Chromatin Organization Eradicate Cellular Stress Resilience to UVA/B Light and Induce Premature Aging

Vasileva

Staneva

Krasteva

et al. 2021

Cells

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Complex interactions among DNA and nuclear proteins maintain genome organization and stability. The nuclear proteins, particularly the histones, organize, compact, and preserve the stability of DNA, but also allow its dynamic reorganization whenever the nuclear processes require access to it. Five histone classes exist and they are evolutionarily conserved among eukaryotes. The linker histones are the fifth class and over time, their role in chromatin has been neglected. Linker histones interact with DNA and the other histones and thus sustain genome stability and nuclear organization. Saccharomyces cerevisiae is a brilliant model for studying linker histones as the gene for it is a single-copy and is non-essential. We, therefore, created a linker histone-free yeast strain using a knockout of the relevant gene and traced the way cells age chronologically. Here we present our results demonstrating that the altered chromatin dynamics during the chronological lifespan of the yeast cells with a mutation in ARP4 (the actin-related protein 4) and without the gene HHO1 for the linker histone leads to strong alterations in the gene expression profiles of a subset of genes involved in DNA repair and autophagy. The obtained results further prove that the yeast mutants have reduced survival upon UVA/B irradiation possibly due to the accelerated decompaction of chromatin and impaired proliferation. Our hypothesis posits that the higher-order chromatin structure and the interactions among chromatin proteins are crucial for the maintenance of chromatin organization during chronological aging under optimal and UVA-B stress conditions.

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“…Following glucose consumption by the yeast culture under non-CR conditions, cells enter the G 0 state and give rise to the high-density Q cell population due to the cell cycle arrest in late G 1 [3,4,[8][9][10]. On the contrary, when the yeast culture under CR conditions consumes glucose, it enters the G 0 state and develops the high-density Q cell population because the cell cycle arrest occurs in early G 1 [14,16,17].…”

Section: Research Papermentioning

confidence: 99%

“…The distinct features exhibited by NQ cells of populations 1, 2 and 3 suggest that the order of their stepwise conversion during chronological aging is NQ 1 → NQ 2 → NQ 3 [ 4 , 16 ]. It is also tempting to speculate that NQ 1 cells are descendants of Q cells [ 4 , 16 ]. It remains unclear how yeast’s chronological aging promotes Q cells’ conversion into NQ 1 cells.…”

Section: Introductionmentioning

confidence: 99%

“…CR affects both criteria of the chronological age-related quiescence decline by the populations of Q and NQ cells. Indeed, CR extends the time these cell populations retain their clonogenicity [ 14 , 16 , 17 ]. Besides, CR slows a chronological aging-associated decline in Q and NQ cells’ ability to synchronously divide if transferred from a nutrient-depleted to a nutrient-rich liquid medium [ 14 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

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