scholarly journals tRNA thiolation links translation to stress responses in Saccharomyces cerevisiae

2015 ◽  
Vol 26 (2) ◽  
pp. 270-282 ◽  
Author(s):  
Jadyn R. Damon ◽  
David Pincus ◽  
Hidde L. Ploegh
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Endoplasmic Reticulum ◽  
Elevated Temperature ◽  
Heat Shock ◽  
Stress Responses ◽  
Wild Type ◽  
Trna Modifications ◽  
Shock Response ◽  
Tightly Coupled

Although tRNA modifications have been well catalogued, the precise functions of many modifications and their roles in mediating gene expression are still being elucidated. Whereas tRNA modifications were long assumed to be constitutive, it is now apparent that the modification status of tRNAs changes in response to different environmental conditions. The URM1 pathway is required for thiolation of the cytoplasmic tRNAs tGluUUC, tGlnUUG, and tLysUUU in Saccharomyces cerevisiae. We demonstrate that URM1 pathway mutants have impaired translation, which results in increased basal activation of the Hsf1-mediated heat shock response; we also find that tRNA thiolation levels in wild-type cells decrease when cells are grown at elevated temperature. We show that defects in tRNA thiolation can be conditionally advantageous, conferring resistance to endoplasmic reticulum stress. URM1 pathway proteins are unstable and hence are more sensitive to changes in the translational capacity of cells, which is decreased in cells experiencing stresses. We propose a model in which a stress-induced decrease in translation results in decreased levels of URM1 pathway components, which results in decreased tRNA thiolation levels, which further serves to decrease translation. This mechanism ensures that tRNA thiolation and translation are tightly coupled and coregulated according to need.

scholarly journals The functional response of the Antarctic bivalve Laternula elliptica to ocean warming and acidification

2021 ◽  
Author(s):  
◽  
Sonja Hempel
Keyword(s):  
Gene Expression ◽  
Elevated Temperature ◽  
Heat Shock ◽  
Physiological Condition ◽  
Ocean Warming ◽  
Hsp70 Gene ◽  
Time Points ◽  
Laternula Elliptica ◽  
Shock Response ◽  
The Antarctic

<p>Marine life is currently under threat from large-scale, long-term changes to the marine environment. Anthropogenic emissions of greenhouse gases, particularly carbon dioxide (CO₂), are causing ongoing change to global marine systems, particularly through ocean warming and acidification. Greenhouse gases in the atmosphere are trapping radiation and heating the entire Earth surface, including the ocean. At the same time, oceanic uptake of CO₂ through absorption by surface waters is altering ocean chemistry, increasing acidity, reducing availability of carbonate ions (CO₃²⁻), and causing increasing dissolution of calcium carbonate (CaCO₃) structures.  Because atmospheric CO₂ diffuses more readily into cold water, the Southern Ocean (SO) will experience ocean acidification in a matter of decades. Warming in the SO is also occurring rapidly and represents a comparatively greater increase in temperature than elsewhere. SO marine fauna have evolved in constant, stable, cold conditions, and as a result are stenothermal and particularly at risk from ocean warming and acidification. The large infaunal bivalve Laternula elliptica is a prevalent keystone species found throughout the Antarctic benthos in high numbers, and contributes significantly to biodeposition and bentho-pelagic coupling.  This thesis examines how L. elliptica adults are affected over medium-term (5-mo) timescales by SO warming and acidification. Adult L. elliptica collected from Cape Evans in McMurdo Sound, Antarctica, were subjected to combinations of temperatures and pHs predicted for the SO by 2050 and 2100 (Temperatures: -1.4°C (control); -0.5°C; +0.5°C. pHs: pH 8.00 (control); pH 7.85; pH 7.65). L. elliptica were assessed at 5 wk and 5 mo to determine their cellular, metabolic, and whole-organism responses to temperature increase and/or pH decrease. Survival parameters such as final survival percentage, survival curves, and time to 50% survival (LD₅₀) were compared among treatments. L. elliptica survival was severely reduced by warming of only 1-2°C above summer ambient temperatures. Physical and physiological condition indices were calculated to assess health, and show changes in shell and body tissue mass. Physical condition stayed similar amongst all treatments at both time points, while physiological condition decreased significantly at 5 mo with elevated temperature. Oxygen (O₂) consumption was measured as a proxy for standard metabolic rate to show whether animals had acclimatised to conditions. O₂ consumption was significantly negatively correlated with physiological condition, and increased, becoming more variable, with both elevated temperature and lowered pH. This indicated that L. elliptica experienced increased metabolic demand in response to these conditions, and there was a general lack of acclimation to these conditions over time. Overall, pH had no significant effect on survival, metabolic rate, or condition. Heat shock protein 70 (HSP70) gene expression levels were measured to provide a preliminary indication of how the heat shock response of L. elliptica responds to both elevated temperature and reduced pH. Lowered pH appeared to stimulate an up-regulation of HSP70 gene expression at both time points, although this was smaller at 5 mo. L. elliptica did not seem to display a heat shock response at environmentally realistic levels of warming.  Overall, warming resulted in lowered survival and condition loss with no sign of acclimation after 5 mo. These responses occurred at smaller degrees of warming than are typically considered lethal for L. elliptica, indicating that successful longer-term maintenance is more thermally limited than short-term survival in this species. While physical (shell) condition was maintained in undersaturated conditions under both elevated temperature and reduced pH, this maintenance occurred alongside increased O₂ demand. Maintaining the aragonitic shell in combination with increased metabolic activity may have contributed to the decline in physiological (body mass) condition observed in L. elliptica. In combination, the results of this experiment indicate that warming of the SO may be more important than ocean acidification to the survival and functioning of adult L. elliptica.</p>

scholarly journals The functional response of the Antarctic bivalve Laternula elliptica to ocean warming and acidification

2021 ◽  
Author(s):  
◽  
Sonja Hempel
Keyword(s):  
Gene Expression ◽  
Elevated Temperature ◽  
Heat Shock ◽  
Physiological Condition ◽  
Ocean Warming ◽  
Hsp70 Gene ◽  
Time Points ◽  
Laternula Elliptica ◽  
Shock Response ◽  
The Antarctic

<p>Marine life is currently under threat from large-scale, long-term changes to the marine environment. Anthropogenic emissions of greenhouse gases, particularly carbon dioxide (CO₂), are causing ongoing change to global marine systems, particularly through ocean warming and acidification. Greenhouse gases in the atmosphere are trapping radiation and heating the entire Earth surface, including the ocean. At the same time, oceanic uptake of CO₂ through absorption by surface waters is altering ocean chemistry, increasing acidity, reducing availability of carbonate ions (CO₃²⁻), and causing increasing dissolution of calcium carbonate (CaCO₃) structures.  Because atmospheric CO₂ diffuses more readily into cold water, the Southern Ocean (SO) will experience ocean acidification in a matter of decades. Warming in the SO is also occurring rapidly and represents a comparatively greater increase in temperature than elsewhere. SO marine fauna have evolved in constant, stable, cold conditions, and as a result are stenothermal and particularly at risk from ocean warming and acidification. The large infaunal bivalve Laternula elliptica is a prevalent keystone species found throughout the Antarctic benthos in high numbers, and contributes significantly to biodeposition and bentho-pelagic coupling.  This thesis examines how L. elliptica adults are affected over medium-term (5-mo) timescales by SO warming and acidification. Adult L. elliptica collected from Cape Evans in McMurdo Sound, Antarctica, were subjected to combinations of temperatures and pHs predicted for the SO by 2050 and 2100 (Temperatures: -1.4°C (control); -0.5°C; +0.5°C. pHs: pH 8.00 (control); pH 7.85; pH 7.65). L. elliptica were assessed at 5 wk and 5 mo to determine their cellular, metabolic, and whole-organism responses to temperature increase and/or pH decrease. Survival parameters such as final survival percentage, survival curves, and time to 50% survival (LD₅₀) were compared among treatments. L. elliptica survival was severely reduced by warming of only 1-2°C above summer ambient temperatures. Physical and physiological condition indices were calculated to assess health, and show changes in shell and body tissue mass. Physical condition stayed similar amongst all treatments at both time points, while physiological condition decreased significantly at 5 mo with elevated temperature. Oxygen (O₂) consumption was measured as a proxy for standard metabolic rate to show whether animals had acclimatised to conditions. O₂ consumption was significantly negatively correlated with physiological condition, and increased, becoming more variable, with both elevated temperature and lowered pH. This indicated that L. elliptica experienced increased metabolic demand in response to these conditions, and there was a general lack of acclimation to these conditions over time. Overall, pH had no significant effect on survival, metabolic rate, or condition. Heat shock protein 70 (HSP70) gene expression levels were measured to provide a preliminary indication of how the heat shock response of L. elliptica responds to both elevated temperature and reduced pH. Lowered pH appeared to stimulate an up-regulation of HSP70 gene expression at both time points, although this was smaller at 5 mo. L. elliptica did not seem to display a heat shock response at environmentally realistic levels of warming.  Overall, warming resulted in lowered survival and condition loss with no sign of acclimation after 5 mo. These responses occurred at smaller degrees of warming than are typically considered lethal for L. elliptica, indicating that successful longer-term maintenance is more thermally limited than short-term survival in this species. While physical (shell) condition was maintained in undersaturated conditions under both elevated temperature and reduced pH, this maintenance occurred alongside increased O₂ demand. Maintaining the aragonitic shell in combination with increased metabolic activity may have contributed to the decline in physiological (body mass) condition observed in L. elliptica. In combination, the results of this experiment indicate that warming of the SO may be more important than ocean acidification to the survival and functioning of adult L. elliptica.</p>

scholarly journals HSFA2 Functions in the Physiological Adaptation of Undifferentiated Plant Cells to Spaceflight

2019 ◽  
Vol 20 (2) ◽  
pp. 390 ◽  
Author(s):  
Agata Zupanska ◽  
Collin LeFrois ◽  
Robert Ferl ◽  
Anna-Lisa Paul
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Stress Responses ◽  
Expression Profiles ◽  
Physiological State ◽  
Heat Shock Factor ◽  
Physiological Adaptation ◽  
Comparative Approach ◽  
Wild Type ◽  
Microarray Gene Expression

Heat Shock Factor A2 (HsfA2) is part of the Heat Shock Factor (HSF) network, and plays an essential role beyond heat shock in environmental stress responses and cellular homeostatic control. Arabidopsis thaliana cell cultures derived from wild type (WT) ecotype Col-0 and a knockout line deficient in the gene encoding HSFA2 (HSFA2 KO) were grown aboard the International Space Station (ISS) to ascertain whether the HSF network functions in the adaptation to the novel environment of spaceflight. Microarray gene expression data were analyzed using a two-part comparative approach. First, genes differentially expressed between the two environments (spaceflight to ground) were identified within the same genotype, which represented physiological adaptation to spaceflight. Second, gene expression profiles were compared between the two genotypes (HSFA2 KO to WT) within the same environment, which defined genes uniquely required by each genotype on the ground and in spaceflight-adapted states. Results showed that the endoplasmic reticulum (ER) stress and unfolded protein response (UPR) define the HSFA2 KO cells’ physiological state irrespective of the environment, and likely resulted from a deficiency in the chaperone-mediated protein folding machinery in the mutant. Results further suggested that additional to its universal stress response role, HsfA2 also has specific roles in the physiological adaptation to spaceflight through cell wall remodeling, signal perception and transduction, and starch biosynthesis. Disabling HsfA2 altered the physiological state of the cells, and impacted the mechanisms induced to adapt to spaceflight, and identified HsfA2-dependent genes that are important to the adaption of wild type cells to spaceflight. Collectively these data indicate a non-thermal role for the HSF network in spaceflight adaptation.

scholarly journals Arabidopsis heat shock transcription factor HSFA7b positively mediates salt stress tolerance by binding to an E-box-like motif to regulate gene expression

2019 ◽  
Vol 70 (19) ◽  
pp. 5355-5374 ◽  
Author(s):  
Dandan Zang ◽  
Jingxin Wang ◽  
Xin Zhang ◽  
Zhujun Liu ◽  
Yucheng Wang
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Heat Shock ◽  
Salt Tolerance ◽  
Stress Responses ◽  
Ion Homeostasis ◽  
Cellulose Synthase ◽  
Regulate Gene Expression ◽  
E Box ◽  
Regulate Gene

Abstract Plant heat shock transcription factors (HSFs) are involved in heat and other abiotic stress responses. However, their functions in salt tolerance are little known. In this study, we characterized the function of a HSF from Arabidopsis, AtHSFA7b, in salt tolerance. AtHSFA7b is a nuclear protein with transactivation activity. ChIP-seq combined with an RNA-seq assay indicated that AtHSFA7b preferentially binds to a novel cis-acting element, termed the E-box-like motif, to regulate gene expression; it also binds to the heat shock element motif. Under salt conditions, AtHSFA7b regulates its target genes to mediate serial physiological changes, including maintaining cellular ion homeostasis, reducing water loss rate, decreasing reactive oxygen species accumulation, and adjusting osmotic potential, which ultimately leads to improved salt tolerance. Additionally, most cellulose synthase-like (CSL) and cellulose synthase (CESA) family genes were inhibited by AtHSFA7b; some of them were randomly selected for salt tolerance characterization, and they were mainly found to negatively modulate salt tolerance. By contrast, some transcription factors (TFs) were induced by AtHSFA7b; among them, we randomly identified six TFs that positively regulate salt tolerance. Thus, AtHSFA7b serves as a transactivator that positively mediates salinity tolerance mainly through binding to the E-box-like motif to regulate gene expression.

The heat shock response: A case study of chromatin dynamics in gene regulation

2013 ◽  
Vol 91 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Sheila S. Teves ◽  
Steven Henikoff
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Control Of Gene Expression ◽  
Pol Ii ◽  
Chromatin Dynamics ◽  
Regulatory Processes ◽  
Shock Response ◽  
Rate Limiting

Recent studies in transcriptional regulation using the Drosophila heat shock response system have elucidated many of the dynamic regulatory processes that govern transcriptional activation and repression. The classic view that the control of gene expression occurs at the point of RNA polymerase II (Pol II) recruitment is now giving way to a more complex outlook of gene regulation. Promoter chromatin dynamics coordinate with transcription factor binding to maintain the promoters of active genes accessible. For a large number of genes, the rate-limiting step in Pol II progression occurs during its initial elongation, where Pol II transcribes 30–50 bp and pauses for further signals. These paused genes have unique genic chromatin architecture and dynamics compared with genes where Pol II recruitment is rate limiting for expression. Further elongation of Pol II along the gene causes nucleosome turnover, a continuous process of eviction and replacement, which suggests a potential mechanism for Pol II transit along a nucleosomal template. In this review, we highlight recent insights into transcription regulation of the heat shock response and discuss how the dynamic regulatory processes involved at each transcriptional stage help to generate faithful yet highly responsive gene expression.

Role of heat shock transcription factor in yeast metallothionein gene expression

1991 ◽  
Vol 11 (7) ◽  
pp. 3676-3681
Author(s):  
W M Yang ◽  
W Gahl ◽  
D Hamer
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Heat Shock ◽  
Gene Transcription ◽  
Heat Shock Factor ◽  
Heat Shock Transcription Factor ◽  
Wild Type ◽  
Promoter Sequences ◽  
Metallothionein Gene ◽  
Upstream Promoter

The induction of Saccharomyces cerevisiae metallothionein gene transcription by Cu and Ag is mediated by the ACE1 transcription factor. In an effort to detect additional stimuli and factors that regulate metallothionein gene transcription, we isolated a Cu-resistant suppressor mutant of an ACE1 deletion strain. Even in the absence of metals, the suppressor mutant exhibited high basal levels of metallothionein gene transcription that required upstream promoter sequences. The suppressor gene was cloned, and its predicted product was shown to correspond to yeast heat shock transcription factor with a single-amino-acid substitution in the DNA-binding domain. The mutant heat shock factor bound strongly to metallothionein gene upstream promoter sequences, whereas wild-type heat shock factor interacted weakly with the same region. Heat treatment led to a slight but reproducible induction of metallothionein gene expression in both wild-type and suppressor strains, and Cd induced transcription in the mutant strain. These studies provide evidence for multiple pathways of metallothionein gene transcriptional regulation in S. cerevisiae.

Repetitive Dictyostelium heat-shock promotor functions in Saccharomyces cerevisiae

1984 ◽  
Vol 4 (4) ◽  
pp. 591-598
Author(s):  
J Cappello ◽  
C Zuker ◽  
H F Lodish
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Nucleotide Sequence ◽  
Dna Sequence ◽  
Base Pair ◽  
Shock Treatment ◽  
Yeast Cells ◽  
Genomic Segment ◽  
Heat Shock Treatment ◽  
Shock Response

The Dictyostelium genome contains 40 copies of a 4.7-kilobase repetitive and apparently transposable DNA sequence (DIRS-1) and about 250 smaller elements that appear to be deletions or rearrangements of DIRS-1. Transcripts of these sequences are induced during differentiation and also by heat shock treatment of growing cells. We showed that one such cloned element, pB41.6 (2.5 kilobases) contains a nucleotide sequence identical to the Drosophila consensus heat shock promotor. To test whether this sequence might indeed control the expression of DIRS-1-related RNAs, we have cloned this genomic segment into yeast cells. In yeast cells, 41.6 directs synthesis of a 1.7-kilobase RNA that is induced at least 10-fold by heat shock. Transcription initiates at about 124 bases 3' of the putative promotor sequence and terminates within the 41.6 insert. A 381-base-pair subclone that contains the putative promotor sequence is sufficient to induce the heat shock response of 41.6 in yeast cells.

A deletion that includes the segment coding for the signal peptidase cleavage site delays release of Saccharomyces cerevisiae acid phosphatase from the endoplasmic reticulum

1986 ◽  
Vol 6 (2) ◽  
pp. 723-729
Author(s):  
R Haguenauer-Tsapis ◽  
M Nagy ◽  
A Ryter
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Endoplasmic Reticulum ◽  
Acid Phosphatase ◽  
Cleavage Site ◽  
Ultrastructural Localization ◽  
Signal Peptidase ◽  
Multicopy Plasmid ◽  
Wild Type ◽  
Sugar Chains ◽  
Pho5 Gene

We studied ultrastructural localization of acid phosphatase in derepressed Saccharomyces cerevisiae cells transformed with a multicopy plasmid carrying either the wild-type PHO5 gene or a PHO5 gene deleted in the region overlapping the signal peptidase cleavage site. Wild-type enzyme was located in the cell wall, as was 50% of the modified protein, which carried high-mannose-sugar chains. The remaining 50% of the protein was active and core glycosylated, and it accumulated in the endoplasmic reticulum cisternae. The signal peptide remained uncleaved in both forms. Cells expressing the modified protein exhibited an exaggerated endoplasmic reticulum with dilated lumen.

Heat shock response of Saccharomyces cerevisiae mutants altered in cyclic AMP-dependent protein phosphorylation

1987 ◽  
Vol 7 (1) ◽  
pp. 244-250
Author(s):  
D Y Shin ◽  
K Matsumoto ◽  
H Iida ◽  
I Uno ◽  
T Ishikawa
Keyword(s):  
Heat Treatment ◽  
Saccharomyces Cerevisiae ◽  
Heat Shock ◽  
Cyclic Amp ◽  
Heat Shock Proteins ◽  
Temperature Shift ◽  
G1 Phase ◽  
Shock Response ◽  
Dependent Protein ◽  
Shock Proteins

When Saccharomyces cerevisiae cells grown at 23 degrees C were transferred to 36 degrees C, they initiated synthesis of heat shock proteins, acquired thermotolerance to a lethal heat treatment given after the temperature shift, and arrested their growth transiently at the G1 phase of the cell division cycle. The bcy1 mutant which resulted in production of cyclic AMP (cAMP)-independent protein kinase did not synthesize the three heat shock proteins hsp72A, hsp72B, and hsp41 after the temperature shift. The bcy1 cells failed to acquire thermotolerance to the lethal heat treatment and were not arrested at the G1 phase after the temperature shift. In contrast, the cyr1-2 mutant, which produced a low level of cAMP, constitutively produced three heat shock proteins and four other proteins without the temperature shift and was resistant to the lethal heat treatment. The results suggest that a decrease in the level of cAMP-dependent protein phosphorylation results in the heat shock response, including elevated synthesis of three heat shock proteins, acquisition of thermotolerance, and transient arrest of the cell cycle.

scholarly journals HrcA and DnaK are important for static and continuous-flow biofilm formation and disinfectant resistance in Listeria monocytogenes

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3782-3790 ◽  
Author(s):  
Stijn van der Veen ◽  
Tjakko Abee
Keyword(s):  
Listeria Monocytogenes ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Peracetic Acid ◽  
Continuous Flow ◽  
Biofilm Formation ◽  
Benzalkonium Chloride ◽  
Wild Type ◽  
Shock Response ◽  
Disinfectant Resistance

The food-borne pathogen Listeria monocytogenes is able to form biofilms in food processing environments. Since biofilms are generally difficult to eradicate during clean-up procedures, they pose a major risk for the food industry. Stress resistance mechanisms involved in L. monocytogenes biofilm formation and disinfectant resistance have, to our knowledge, not been identified thus far. In this study, we investigated the role of hrcA, which encodes the transcriptional regulator of the class I heat-shock response, and dnaK, which encodes a class I heat-shock response chaperone protein, in static and continuous-flow biofilm formation and resistance against benzalkonium chloride and peracetic acid. Induction of both hrcA and dnaK during continuous-flow biofilm formation was observed using quantitative real-time PCR and promoter reporters. Furthermore, in-frame deletion and complementation mutants of hrcA and dnaK revealed that HrcA and DnaK are required to reach wild-type levels of both static and continuous-flow biofilms. Finally, disinfection treatments of planktonic-grown cells and suspended static and continuous-flow biofilm cells of wild-type and mutants showed that HrcA and DnaK are important for resistance against benzalkonium chloride and peracetic acid. In conclusion, our study revealed that HrcA and DnaK are important for L. monocytogenes biofilm formation and disinfectant resistance.

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