High-Resolution Profiling of Stationary-Phase Survival Reveals Yeast Longevity Factors and Their Genetic Interactions

Garay, Erika; Campos, Sergio; Cruz, Jorge Gonzalez de la; Gaspar, Ana P.; Jinich, Adrián; DeLuna, Alexander

doi:10.1371/journal.pgen.1004168

Cited by 87 publications

(122 citation statements)

References 79 publications

(99 reference statements)

Supporting

Mentioning

113

Contrasting

Order By: Relevance

“…S4c). In this regard, the screen performed in ammonium was carried out in a buffered medium (Garay et al., 2014), while the ones presented here are not, implying that some of the condition‐specific effects could be due to different pH in the stationary‐phase cultures. In conclusion, these comparative analyses suggest that, while some gene deletions have diminished or enhanced lifespan extension only under specific conditions, most DR genes influence the lifespan response to nutrient limitation regardless of the nitrogen source used to model dietary restriction.…”

Section: Resultscontrasting

confidence: 63%

“…Specifically, we used data from a previously reported genomewide screen performed in 2% glucose SC medium with ammonium sulfate as the sole nitrogen source (Garay et al., 2014), to obtain a new relative lifespan extension value for each knockout, LE GABA/NH4 . We observed a strong skew in the distribution of LE GABA/NH4 values, for both sets DR genes with diminished‐ LE ( p < 10 −28 , one‐tailed Wilcoxon ranked‐sum test) or enhanced‐ LE ( p < 10 −34 ) using the GABA/glutamine comparison (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Fluorescent single‐gene deletion strains are prototrophic haploids ( MAT a xxx Δ ::kanMX4 PDC1‐mcherry‐CaURA3MX4 can1 Δ :STE2pr‐SpHIS5 lyp1 Δ his3 Δ 1 ura3 Δ 0 LEU2 ) derived from crossing the MAT α YEG01‐RFP SGA‐starter with 4,340 viable deletion strains from the MAT a BY4741 collection from the Saccharomyces Genome Deletion Project (Garay et al., 2014). All de novo single‐gene deletions were generated in the YEG01‐RFP parental strain ( MAT α PDC1‐mcherry‐CaURA3MX4 can1 Δ :STE2pr‐SpHIS5 lyp1 Δ his3 Δ 1 ura3 Δ 0 LEU2 ) by direct gene replacement with the natMX4 module conferring resistance to clonNAT.…”

Section: Methodsmentioning

confidence: 99%

“…For instance, a recent systematic study of replicative lifespan of most viable deletion strains revealed that translation, the SAGA complex, and the TCA cycle mediate longevity (McCormick et al., 2015). Several studies have aimed to estimate the stationary‐phase survival of single deletion mutants in parallel (Fabrizio et al., 2010; Garay et al., 2014; Gresham et al., 2011; Matecic et al., 2010; Powers et al., 2006), showing that autophagy, vacuolar protein sorting, regulation of translation, purine metabolism, chromatin remodeling, and the SWR1 complex are major determinants of longevity. However, we are still missing a direct comparison of the lifespan effects of such gene deletions under nutrient‐rich and restricted conditions that would allow to systematically address the mechanisms of longevity by dietary restriction.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, we compared the CLS of a collection of 3,718 knockout mutants aged in media with glutamine (nonrestricted) or γ‐aminobutyric acid (GABA, dietary‐restricted) nitrogen source, for which we used a high‐resolution parallel phenotyping assay (Garay et al., 2014). These screens revealed that at least 473 genes have a role in lifespan extension by GABA.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

et al. 2018

Self Cite

View full text Add to dashboard Cite

SummaryDietary restriction is arguably the most promising nonpharmacological intervention to extend human life and health span. Yet, only few genetic regulators mediating the cellular response to dietary restriction are known, and the question remains which other regulatory factors are involved. Here, we measured at the genomewide level the chronological lifespan of Saccharomyces cerevisiae gene deletion strains under two nitrogen source regimens, glutamine (nonrestricted) and γ‐aminobutyric acid (restricted). We identified 473 mutants with diminished or enhanced extension of lifespan. Functional analysis of such dietary restriction genes revealed novel processes underlying longevity by the nitrogen source quality, which also allowed us to generate a prioritized catalogue of transcription factors orchestrating the dietary restriction response. Importantly, deletions of transcription factors Msn2, Msn4, Snf6, Tec1, and Ste12 resulted in diminished lifespan extension and defects in cell cycle arrest upon nutrient starvation, suggesting that regulation of the cell cycle is a major mechanism of chronological longevity. We further show that STE12 overexpression is enough to extend lifespan, linking the pheromone/invasive growth pathway with cell survivorship. Our global picture of the genetic players of longevity by dietary restriction highlights intricate regulatory cross‐talks in aging cells.

show abstract

Section: Resultscontrasting

confidence: 63%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

Cellular quiescence in budding yeast

Sun

Gresham

2021

Yeast

View full text Add to dashboard Cite

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

show abstract

Old yeasts, young beer—The industrial relevance of yeast chronological life span

Wauters

Britton

Verstrepen

2021

Yeast

View full text Add to dashboard Cite

Much like other living organisms, yeast cells have a limited life span, in terms of both the maximal length of time a cell can stay alive (chronological life span) and the maximal number of cell divisions it can undergo (replicative life span). Over the past years, intensive research revealed that the life span of yeast depends on both the genetic background of the cells and environmental factors. Specifically, the presence of stress factors, reactive oxygen species, and the availability of nutrients profoundly impact life span, and signaling cascades involved in the response to these factors, including the target of rapamycin (TOR) and cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathways, play a central role. Interestingly, yeast life span also has direct implications for its use in industrial processes. In beer brewing, for example, the inoculation of finished beer with live yeast cells, a process called "bottle conditioning" helps improve the product's shelf life by clearing undesirable carbonyl compounds such as furfural and 2-methylpropanal that cause staling. However, this effect depends on the reductive metabolism of living cells and is thus inherently limited by the cells' chronological life span. Here, we review the mechanisms underlying chronological life span in yeast. We also discuss how this insight connects to industrial observations and ultimately opens new routes towards superior industrial yeasts that can help improve a product's shelf life and thus contribute to a more sustainable industry.

show abstract

High-Resolution Profiling of Stationary-Phase Survival Reveals Yeast Longevity Factors and Their Genetic Interactions

Cited by 87 publications

References 79 publications

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast

Cellular quiescence in budding yeast

Old yeasts, young beer—The industrial relevance of yeast chronological life span

Contact Info

Product

Resources

About