scholarly journals Global Gene Expression Responses of Fission Yeast to Ionizing Radiation

2004 ◽  
Vol 15 (2) ◽  
pp. 851-860 ◽  
Author(s):  
Adam Watson ◽  
Juan Mata ◽  
Jürg Bähler ◽  
Anthony Carr ◽  
Tim Humphrey
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Stress Response ◽  
Ionizing Radiation ◽  
Environmental Stress ◽  
Fission Yeast ◽  
Transcriptional Response ◽  
Global Gene Expression ◽  
Environmental Stress Response ◽  
Stress Response Genes

A coordinated transcriptional response to DNA-damaging agents is required to maintain genome stability. We have examined the global gene expression responses of the fission yeast Schizosaccharomyces pombe to ionizing radiation (IR) by using DNA microarrays. We identified ∼200 genes whose transcript levels were significantly altered at least twofold in response to 500 Gy of gamma IR in a temporally defined manner. The majority of induced genes were core environmental stress response genes, whereas the remaining genes define a transcriptional response to DNA damage in fission yeast. Surprisingly, few DNA repair and checkpoint genes were transcriptionally modulated in response to IR. We define a role for the stress-activated mitogen-activated protein kinase Sty1/Spc1 and the DNA damage checkpoint kinase Rad3 in regulating core environmental stress response genes and IR-specific response genes, both independently and in concert. These findings suggest a complex network of regulatory pathways coordinate gene expression responses to IR in eukaryotes.

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 Caffeine Stabilises Fission Yeast Wee1 in a Rad24-Dependent Manner but Attenuates Its Expression in Response to DNA Damage

2020 ◽  
Vol 8 (10) ◽  
pp. 1512
Author(s):  
John P. Alao ◽  
Johanna Johansson-Sjölander ◽  
Charalampos Rallis ◽  
Per Sunnerhagen
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Stress Response ◽  
Environmental Stress ◽  
Cell Cycle Progression ◽  
Dependent Manner ◽  
Environmental Stress Response ◽  
Cycle Progression ◽  
Dna Damage Checkpoints ◽  
Wee1 Kinase

The widely consumed neuroactive compound caffeine has generated much interest due to its ability to override the DNA damage and replication checkpoints. Previously Rad3 and its homologues was thought to be the target of caffeine’s inhibitory activity. Later findings indicate that the Target of Rapamycin Complex 1 (TORC1) is the preferred target of caffeine. Effective Cdc2 inhibition requires both the activation of the Wee1 kinase and inhibition of the Cdc25 phosphatase. The TORC1, DNA damage, and environmental stress response pathways all converge on Cdc25 and Wee1. We previously demonstrated that caffeine overrides DNA damage checkpoints by modulating Cdc25 stability. The effect of caffeine on cell cycle progression resembles that of TORC1 inhibition. Furthermore, caffeine activates the Sty1 regulated environmental stress response. Caffeine may thus modulate multiple signalling pathways that regulate Cdc25 and Wee1 levels, localisation and activity. Here we show that the activity of caffeine stabilises both Cdc25 and Wee1. The stabilising effect of caffeine and genotoxic agents on Wee1 was dependent on the Rad24 chaperone. Interestingly, caffeine inhibited the accumulation of Wee1 in response to DNA damage. Caffeine may modulate cell cycle progression through increased Cdc25 activity and Wee1 repression following DNA damage via TORC1 inhibition, as TORC1 inhibition increased DNA damage sensitivity.

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 Plant Core Environmental Stress Response Genes Are Systemically Coordinated during Abiotic Stresses

2013 ◽  
Vol 14 (4) ◽  
pp. 7617-7641 ◽  
Author(s):  
Achim Hahn ◽  
Joachim Kilian ◽  
Anne Mohrholz ◽  
Friederike Ladwig ◽  
Florian Peschke ◽  
...  
Keyword(s):  
Stress Response ◽  
Environmental Stress ◽  
Abiotic Stresses ◽  
Environmental Stress Response ◽  
Stress Response Genes

scholarly journals Set4 regulates stress response genes and coordinates histone deacetylases within yeast subtelomeres

2021 ◽  
Vol 4 (12) ◽  
pp. e202101126
Author(s):  
Yogita Jethmalani ◽  
Khoa Tran ◽  
Maraki Y Negesse ◽  
Winny Sun ◽  
Mark Ramos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Histone Deacetylases ◽  
Regulation Of Gene Expression ◽  
Global Gene Expression ◽  
Stress Response Genes ◽  
Hypoxic Conditions ◽  
Global Gene Expression Analysis ◽  
Sir Complex ◽  
Stress Dependent

The yeast chromatin protein Set4 is a member of the Set3-subfamily of SET domain proteins which play critical roles in the regulation of gene expression in diverse developmental and environmental contexts. We previously reported that Set4 promotes survival during oxidative stress and regulates expression of stress response genes via stress-dependent chromatin localization. In this study, global gene expression analysis and investigation of histone modification status identified a role for Set4 in maintaining gene repressive mechanisms within yeast subtelomeres under both normal and stress conditions. We show that Set4 works in a partially overlapping pathway to the SIR complex and the histone deacetylase Rpd3 to maintain proper levels of histone acetylation and expression of stress response genes encoded in subtelomeres. This role for Set4 is particularly critical for cells under hypoxic conditions, where the loss of Set4 decreases cell fitness and cell wall integrity. These findings uncover a new regulator of subtelomeric chromatin that is key to stress defense pathways and demonstrate a function for Set4 in regulating repressive, heterochromatin-like environments.

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 Caffeine stabilises fission yeast Wee1 in a Rad24-dependent manner but attenuates its expression in response to DNA damage identifying a putative role for TORC1 in mediating its effects on cell cycle progression

2020 ◽  
Author(s):  
John P. Alao ◽  
Johanna Johansson-Sjölander ◽  
Charalampos Rallis ◽  
Per Sunnerhagen
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Stress Response ◽  
Environmental Stress ◽  
Cell Cycle Progression ◽  
Dependent Manner ◽  
Environmental Stress Response ◽  
Cycle Progression ◽  
Dna Damage Checkpoints ◽  
Wee1 Kinase

AbstractThe widely consumed neuroactive compound caffeine has generated much interest due to its ability to override the DNA damage and replication checkpoints. Previously Rad3 and its homologues was thought to be the target of caffeine’s inhibitory activity. Later findings indicate that the Target of Rapamycin Complex 1 (TORC1) is the preferred target of caffeine. Effective Cdc2 inhibition requires both the activation of the Wee1 kinase and inhibition of the Cdc25 phosphatase. The TORC1, DNA damage, and environmental stress response pathways all converge on Cdc25 and Wee1. We previously demonstrated that caffeine overrides DNA damage checkpoints by modulating Cdc25 stability. The effect of caffeine on cell cycle progression resembles that of TORC1 inhibition. Furthermore, caffeine activates the Sty1 regulated environmental stress response. Caffeine may thus modulate multiple signalling pathways that regulate Cdc25 and Wee1 levels, localisation and activity. Here we show that the activity of caffeine stabilises both Cdc25 and Wee1. The stabilising effect of caffeine and genotoxic agents on Wee1 was dependent on the Rad24 chaperone. Interestingly, caffeine inhibited the accumulation of Wee1 in response to DNA damage. Caffeine therefore modulates cell cycle progression contextually through increased Cdc25 activity and Wee1 repression following DNA damage via TORC1 inhibition.

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 A dataset to explore kinase control of environmental stress responsive transcription

2019 ◽  
Author(s):  
Kieran Mace ◽  
Joanna Krakowiak ◽  
Hana El-Samad ◽  
David Pincus
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Environmental Stress ◽  
Environmental Conditions ◽  
Target Genes ◽  
Growth Control ◽  
Gene Expression Signature ◽  
Negative Regulator ◽  
Cellular Stress Response ◽  
Environmental Stress Response

ABSTRACTCells respond to changes in environmental conditions by activating signal transduction pathways and gene expression programs. Here we present a dataset to explore the relationship between environmental stresses, kinases, and global gene expression in yeast. We subjected 28 drug-sensitive kinase mutants to 10 environmental conditions in the presence of inhibitor and performed mRNA deep sequencing. With these data, we reconstructed canonical stress pathways and identified examples of crosstalk among pathways. The data also implicated numerous kinases in novel environment-specific roles. However, rather than regulating dedicated sets of target genes, individual kinases tuned the magnitude of induction of the environmental stress response (ESR) – a gene expression signature shared across the set of perturbations – in environment-specific ways. This suggests that the ESR integrates inputs from multiple sensory kinases to modulate gene expression and growth control. As an example, we provide experimental evidence that the high osmolarity glycerol pathway is a constitutive negative regulator of protein kinase A, a known inhibitor of the ESR. These results elaborate the central axis of cellular stress response signaling.

scholarly journals Set4 coordinates the activity of histone deacetylases and regulates stress-responsive gene expression within subtelomeric regions in yeast

2021 ◽  
Author(s):  
Yogita Jethmalani ◽  
Khoa Tran ◽  
Deepika Jaiswal ◽  
Meagan Jezek ◽  
Mark Ramos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Histone Deacetylases ◽  
Regulation Of Gene Expression ◽  
Global Gene Expression ◽  
Growth Conditions ◽  
Stress Response Genes ◽  
Hypoxic Conditions ◽  
Sir Complex ◽  
Stress Dependent

The yeast chromatin protein Set4 is a member of the Set3-subfamily of SET domain proteins which play critical roles in the regulation of gene expression in diverse developmental and environmental contexts, although they appear to lack methyltransferase activity. The molecular functions of Set4 are relatively unexplored, likely due to its low abundance in standard growth conditions. We previously reported that Set4 promotes survival during oxidative stress and regulates expression of stress response genes via stress-dependent chromatin localization. In this study, global gene expression analysis and investigation of histone modification status has revealed a role for Set4 in maintaining gene repressive mechanisms within yeast subtelomeres under both normal and stress conditions. We show that Set4 works in a partially overlapping pathway to the SIR complex and the histone deacetylase Rpd3 to maintain proper levels of histone acetylation and expression of stress response genes encoded in subtelomeres. This role for Set4 is particularly critical for cells under hypoxic conditions, and the loss of Set4 decreases cell fitness and cell wall integrity in hypoxia. These findings uncover a new regulator of subtelomeric chromatin that is key to stress defense pathways and demonstrate a function for yeast Set4 in regulating repressive, heterochromatin-like environments.

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