Oxidative stress triggers aggregation of GFP-tagged Hsp31p, the budding yeast environmental stress response chaperone, and glyoxalase III

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.

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Cold Adaptation in Budding Yeast

Molecular Biology of the Cell ◽

10.1091/mbc.e04-03-0167 ◽

2004 ◽

Vol 15 (12) ◽

pp. 5492-5502 ◽

Cited By ~ 120

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.

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Adenine starvation is signalled through environmental stress response system in budding yeast Saccharomyces cerevisiae

Environmental and Experimental Biology ◽

10.22364/eeb.15.29 ◽

2017 ◽

Keyword(s):

Saccharomyces Cerevisiae ◽

Stress Response ◽

Environmental Stress ◽

Budding Yeast ◽

Environmental Stress Response ◽

Yeast Saccharomyces Cerevisiae ◽

Response System ◽

Stress Response System

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Generally Stressed Out Bacteria: Environmental Stress Response Mechanisms in Gram-Positive Bacteria

Integrative and Comparative Biology ◽

10.1093/icb/icaa002 ◽

2020 ◽

Vol 60 (1) ◽

pp. 126-133

Author(s):

Carla Y Bonilla

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Environmental Stress ◽

Bacterial Species ◽

Dynamic Environments ◽

System Level ◽

Environmental Stress Response ◽

Gram Positive ◽

Bacterial Physiology ◽

Wide Range

Abstract The ability to monitor the environment for toxic chemical and physical disturbances is essential for bacteria that live in dynamic environments. The fundamental sensing mechanisms and physiological responses that allow bacteria to thrive are conserved even if the molecular components of these pathways are not. The bacterial general stress response (GSR) represents a conceptual model for how one pathway integrates a wide range of environmental signals, and how a generalized system with broad molecular responses is coordinated to promote survival likely through complementary pathways. Environmental stress signals such as heat, osmotic stress, and pH changes are received by sensor proteins that through a signaling cascade activate the sigma factor, SigB, to regulate over 200 genes. Additionally, the GSR plays an important role in stress priming that increases bacterial fitness to unrelated subsequent stressors such as oxidative compounds. While the GSR response is implicated during oxidative stress, the reason for its activation remains unknown and suggests crosstalk between environmental and oxidative stress sensors and responses to coordinate antioxidant functions. Systems levels studies of cellular responses such as transcriptomes, proteomes, and metabolomes of stressed bacteria and single-cell analysis could shed light into the regulated functions that protect, remediate, and minimize damage during dynamic environments. This perspective will focus on fundamental stress sensing mechanisms and responses in Gram-positive bacterial species to illustrate their commonalities at the molecular and physiological levels; summarize exciting directions; and highlight how system-level approaches can help us understand bacterial physiology.

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The environmental stress response causes ribosome loss in aneuploid yeast cells

10.1101/2020.03.25.008540 ◽

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.

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