scholarly journals Cold Adaptation in Budding Yeast

2004 ◽  
Vol 15 (12) ◽  
pp. 5492-5502 ◽  
Author(s):  
Babette Schade ◽  
Gregor Jansen ◽  
Malcolm Whiteway ◽  
Karl D. Entian ◽  
David Y. Thomas
Keyword(s):  
Stress Response ◽  
Environmental Stress ◽  
Stress Responses ◽  
Budding Yeast ◽  
Transcriptional Response ◽  
Transcript Abundance ◽  
Yeast Cells ◽  
Environmental Stress Response ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cold Response

We have determined the transcriptional response of the budding yeast Saccharomyces cerevisiae to cold. Yeast cells were exposed to 10°C for different lengths of time, and DNA microarrays were used to characterize the changes in transcript abundance. Two distinct groups of transcriptionally modulated genes were identified and defined as the early cold response and the late cold response. A detailed comparison of the cold response with various environmental stress responses revealed a substantial overlap between environmental stress response genes and late cold response genes. In addition, the accumulation of the carbohydrate reserves trehalose and glycogen is induced during late cold response. These observations suggest that the environmental stress response (ESR) occurs during the late cold response. The transcriptional activators Msn2p and Msn4p are involved in the induction of genes common to many stress responses, and we show that they mediate the stress response pattern observed during the late cold response. In contrast, classical markers of the ESR were absent during the early cold response, and the transcriptional response of the early cold response genes was Msn2p/Msn4p independent. This implies that the cold-specific early response is mediated by a different and as yet uncharacterized regulatory mechanism.

scholarly journals The environmental stress response causes ribosome loss in aneuploid yeast cells

2020 ◽  
Vol 117 (29) ◽  
pp. 17031-17040 ◽  
Author(s):  
Allegra Terhorst ◽  
Arzu Sandikci ◽  
Abigail Keller ◽  
Charles A. Whittaker ◽  
Maitreya J. Dunham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Stationary Phase ◽  
Environmental Stress ◽  
Budding Yeast ◽  
Expression Patterns ◽  
Yeast Cells ◽  
Specific Gene ◽  
Environmental Stress Response ◽  
Cellular Stresses

Aneuploidy, a condition characterized by whole chromosome gains and losses, is often associated with significant cellular stress and decreased fitness. However, how cells respond to the aneuploid state has remained controversial. In aneuploid budding yeast, two opposing gene-expression patterns have been reported: the “environmental stress response” (ESR) and the “common aneuploidy gene-expression” (CAGE) signature, in which many ESR genes are oppositely regulated. Here, we investigate this controversy. We show that the CAGE signature is not an aneuploidy-specific gene-expression signature but the result of normalizing the gene-expression profile of actively proliferating aneuploid cells to that of euploid cells grown into stationary phase. Because growth into stationary phase is among the strongest inducers of the ESR, the ESR in aneuploid cells was masked when stationary phase euploid cells were used for normalization in transcriptomic studies. When exponentially growing euploid cells are used in gene-expression comparisons with aneuploid cells, the CAGE signature is no longer evident in aneuploid cells. Instead, aneuploid cells exhibit the ESR. We further show that the ESR causes selective ribosome loss in aneuploid cells, providing an explanation for the decreased cellular density of aneuploid cells. We conclude that aneuploid budding yeast cells mount the ESR, rather than the CAGE signature, in response to aneuploidy-induced cellular stresses, resulting in selective ribosome loss. We propose that the ESR serves two purposes in aneuploid cells: protecting cells from aneuploidy-induced cellular stresses and preventing excessive cellular enlargement during slowed cell cycles by down-regulating translation capacity.

scholarly journals Oxidative Stress Responses and Nutrient Starvation in MCHM Treated Saccharomyces cerevisiae

2020 ◽  
Author(s):  
Michael C. Ayers ◽  
Zachary N. Sherman ◽  
Jennifer E.G. Gallagher
Keyword(s):  
Amino Acid ◽  
Stress Response ◽  
Environmental Stress ◽  
Stress Responses ◽  
Aromatic Amino Acid ◽  
Time Course ◽  
Mitochondrial Gene ◽  
Yeast Cells ◽  
Nutrient Deprivation ◽  
Environmental Stress Response

AbstractIn 2014, the coal cleaning chemical 4-methylcyclohexane methanol (MCHM) spilled into the water supply for 300,000 West Virginians. Initial toxicology tests showed relatively mild results, but the underlying effects on cellular biology were underexplored. Treated wildtype yeast cells grew poorly, but there was only a small decrease in cell viability. Cell cycle analysis revealed an absence of cells in S phase within thirty minutes of treatment. Cells accumulated in G1 over a six-hour time course, indicating arrest instead of death. A genetic screen of the haploid knockout collection revealed 329 high confidence genes required for optimal growth in MCHM. These genes encode three major cell processes: mitochondrial gene expression/translation, the vacuolar ATPase, and aromatic amino acid biosynthesis. The transcriptome showed an upregulation of pleiotropic drug response genes and amino acid biosynthetic genes and downregulation in ribosome biosynthesis. Analysis of these datasets pointed to environmental stress response activation upon treatment. Overlap in datasets included the aromatic amino acid genes ARO1, ARO3, and four of the five TRP genes. This implicated nutrient deprivation as the signal for stress response. Excess supplementation of nutrients and amino acids did not improve growth on MCHM, so the source of nutrient deprivation signal is still unclear. Reactive oxygen species and DNA damage were directly detected with MCHM treatment, but timepoints showed these accumulated slower than cells arrested. We propose that wildtype cells arrest from nutrient deprivation and survive, accumulating oxidative damage through the implementation of robust environmental stress responses.

scholarly journals The environmental stress response causes ribosome loss in aneuploid yeast cells

2020 ◽  
Author(s):  
Allegra Terhorst ◽  
Arzu Sandikci ◽  
Abigail Keller ◽  
Charles A. Whittaker ◽  
Maitreya J. Dunham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Stationary Phase ◽  
Environmental Stress ◽  
Budding Yeast ◽  
Expression Patterns ◽  
Yeast Cells ◽  
Specific Gene ◽  
Environmental Stress Response ◽  
Cellular Stresses

AbstractAneuploidy, a condition characterized by whole chromosome gains and losses, is often associated with significant cellular stress and decreased fitness. However, how cells respond to the aneuploid state has remained controversial. In aneuploid budding yeast, two opposing gene expression patterns have been reported: the “environmental stress response” (ESR) and the “common aneuploidy gene-expression” (CAGE) signature, in which many ESR genes are oppositely regulated. Here, we investigate and bring clarity to this controversy. We show that the CAGE signature is not an aneuploidy-specific gene expression signature but the result of normalizing the gene expression profile of actively proliferating aneuploid cells to that of euploid cells grown into stationary phase. Because growth into stationary phase is amongst the strongest inducers of the ESR, the ESR in aneuploid cells was masked when stationary phase euploid cells were used for normalization in transcriptomic studies. When exponentially growing euploid cells are used in gene expression comparisons with aneuploid cells, the CAGE signature is no longer evident in aneuploid cells. Instead, aneuploid cells exhibit the ESR. We further show that the ESR causes selective ribosome loss in aneuploid cells, providing an explanation for the decreased cellular density of aneuploid cells. We conclude that aneuploid budding yeast cells mount the ESR, rather than the CAGE signature, in response to aneuploidy-induced cellular stresses, resulting in selective ribosome loss. We propose that the ESR serves two purposes in aneuploid cells: protecting cells from aneuploidy-induced cellular stresses and preventing excessive cellular enlargement during slowed cell cycles by downregulating translation capacity.

scholarly journals The environmental stress response regulates ribosome content in cell cycle-arrested S. cerevisiae

2021 ◽  
Author(s):  
Allegra Terhorst ◽  
Arzu Sandikci ◽  
Gabriel E. Neurohr ◽  
Charles A. Whittaker ◽  
Tamás Szórádi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stress Response ◽  
Environmental Stress ◽  
Cell Cycle Progression ◽  
Transcriptional Response ◽  
Biomass Accumulation ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Environmental Stress Response ◽  
Pka Pathway

Temperature sensitive cell division cycle (cdc-ts) cells are unable to progress through the cell cycle at the restrictive temperature due to mutations in genes essential to cell cycle progress. Cells harboring cdc-ts mutations increase in cell volume upon arrest but eventually stop growing. We found that this attenuation in growth was due to selective downregulation of ribosome concentration. We saw similar ribosome downregulation in cells arrested in the cell cycle through alpha factor addition, rapamycin addition, and entrance into stationary phase. In all cell cycle arrests studied, cells activated the Environmental Stress Response (ESR), a key transcriptional response to many stressors in S. cerevisiae. When we combined cell cycle arrest with hyperactivation of the Ras/PKA pathway, ESR activation was prevented, cells were unable to downregulate their ribosomes, and cell viability was decreased. Our work uncovers a key role for the environmental stress response in coupling cell cycle progression to biomass accumulation.

scholarly journals Differences in environmental stress response among yeasts is consistent with species-specific lifestyles

2016 ◽  
Vol 27 (10) ◽  
pp. 1694-1705 ◽  
Author(s):  
Christian Brion ◽  
David Pflieger ◽  
Sirine Souali-Crespo ◽  
Anne Friedrich ◽  
Joseph Schacherer
Keyword(s):  
Stress Response ◽  
Environmental Stress ◽  
Regulatory Networks ◽  
Large Data ◽  
Environmental Stress Response ◽  
Yeast Saccharomyces Cerevisiae ◽  
Data Set ◽  
General Rules ◽  
Evolution Of Gene Regulation ◽  
Species Specific

Defining how organisms respond to environmental change has always been an important step toward understanding their adaptive capacity and physiology. Variation in transcription during stress has been widely described in model species, especially in the yeast Saccharomyces cerevisiae, which helped to shape general rules regarding how cells cope with environmental constraints, as well as to decipher the functions of many genes. Comparison of the environmental stress response (ESR) across species is essential to obtaining better insight into the common and species-specific features of stress defense. In this context, we explored the transcriptional landscape of the yeast Lachancea kluyveri (formerly Saccharomyces kluyveri) in response to diverse stresses, using RNA sequencing. We investigated variation in gene expression and observed a link between genetic plasticity and environmental sensitivity. We identified the ESR genes in this species and compared them to those already found in S. cerevisiae. We observed common features between the two species, as well as divergence in the regulatory networks involved. Of interest, some changes were related to differences in species lifestyle. Thus we were able to decipher how adaptation to stress has evolved among different yeast species. Finally, by analyzing patterns of coexpression, we were able to propose potential biological functions for 42% of genes and also annotate 301 genes for which no function could be assigned by homology. This large data set allowed for the characterization of the evolution of gene regulation and provides an efficient tool for assessing gene function.

scholarly journals Oxidative Stress Responses and Nutrient Starvation in MCHM Treated Saccharomyces cerevisiae

2020 ◽  
Vol 10 (12) ◽  
pp. 4665-4678
Author(s):  
Michael C. Ayers ◽  
Zachary N. Sherman ◽  
Jennifer E. G. Gallagher
Keyword(s):  
Amino Acid ◽  
Stress Response ◽  
Environmental Stress ◽  
Stress Responses ◽  
Aromatic Amino Acid ◽  
Time Course ◽  
Mitochondrial Gene ◽  
Yeast Cells ◽  
Nutrient Deprivation ◽  
Link Type

In 2014, the coal cleaning chemical 4-methylcyclohexane methanol (MCHM) spilled into the water supply for 300,000 West Virginians. Initial toxicology tests showed relatively mild results, but the underlying effects on cellular biology were underexplored. Treated wildtype yeast cells grew poorly, but there was only a small decrease in cell viability. Cell cycle analysis revealed an absence of cells in S phase within thirty minutes of treatment. Cells accumulated in G1 over a six-hour time course, indicating arrest instead of death. A genetic screen of the haploid knockout collection revealed 329 high confidence genes required for optimal growth in MCHM. These genes encode three major cell processes: mitochondrial gene expression/translation, the vacuolar ATPase, and aromatic amino acid biosynthesis. The transcriptome showed an upregulation of pleiotropic drug response genes and amino acid biosynthetic genes and downregulation in ribosome biosynthesis. Analysis of these datasets pointed to environmental stress response activation upon treatment. Overlap in datasets included the aromatic amino acid genes ARO1, ARO3, and four of the five TRP genes. This implicated nutrient deprivation as the signal for stress response. Excess supplementation of nutrients and amino acids did not improve growth on MCHM, so the source of nutrient deprivation signal is still unclear. Reactive oxygen species and DNA damage were directly detected with MCHM treatment, but timepoints showed these accumulated slower than cells arrested. We propose that wildtype cells arrest from nutrient deprivation and survive, accumulating oxidative damage through the implementation of robust environmental stress responses.

scholarly journals Histone Methylation and Memory of Environmental Stress

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 339 ◽  
Author(s):  
Paola Fabrizio ◽  
Steven Garvis ◽  
Francesca Palladino
Keyword(s):  
Environmental Stress ◽  
Histone Methylation ◽  
Stress Responses ◽  
Transcriptional Response ◽  
Epigenetic Inheritance ◽  
Yeast Saccharomyces Cerevisiae ◽  
Post Translational Modifications ◽  
Wide Range ◽  
Transcriptional Memory ◽  
Response To Stress

Cellular adaptation to environmental stress relies on a wide range of tightly controlled regulatory mechanisms, including transcription. Changes in chromatin structure and organization accompany the transcriptional response to stress, and in some cases, can impart memory of stress exposure to subsequent generations through mechanisms of epigenetic inheritance. In the budding yeast Saccharomyces cerevisiae, histone post-translational modifications, and in particular histone methylation, have been shown to confer transcriptional memory of exposure to environmental stress conditions through mitotic divisions. Recent evidence from Caenorhabditis elegans also implicates histone methylation in transgenerational inheritance of stress responses, suggesting a more widely conserved role in epigenetic memory.

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