scholarly journals The Power of Stress: The Telo-Hormesis Hypothesis

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1156
Author(s):  
Maria Sol Jacome Burbano ◽  
Eric Gilson
Keyword(s):  
Stress Response ◽  
Mutation Rates ◽  
Basic Principles ◽  
Beneficial Effects ◽  
Response To Stress ◽  
Telomere Biology ◽  
Telomere Structure ◽  
Structure And Functions

Adaptative response to stress is a strategy conserved across evolution to promote survival. In this context, the groundbreaking findings of Miroslav Radman on the adaptative value of changing mutation rates opened new avenues in our understanding of stress response. Inspired by this work, we explore here the putative beneficial effects of changing the ends of eukaryotic chromosomes, the telomeres, in response to stress. We first summarize basic principles in telomere biology and then describe how various types of stress can alter telomere structure and functions. Finally, we discuss the hypothesis of stress-induced telomere signaling with hormetic effects.

Thermal and Starvation Stress Response of Escherichia coli O157:H7 Isolates Selected from Agricultural Environments

2016 ◽  
Vol 79 (10) ◽  
pp. 1673-1679 ◽  
Author(s):  
ACHYUT ADHIKARI ◽  
ANDY BARY ◽  
CRAIG COGGER ◽  
CALEB JAMES ◽  
GÜLHAN ÜNLÜ ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Heat Stress ◽  
Stress Response ◽  
Weibull Model ◽  
Stress Conditions ◽  
Inactivation Kinetics ◽  
Escherichia Coli O157 ◽  
Starvation Stress ◽  
E Coli ◽  
Response To Stress

ABSTRACT Pathogens exposed to agricultural production environments are subject to multiple stresses that may alter their survival under subsequent stress conditions. The objective of this study was to examine heat and starvation stress response of Escherichia coli O157:H7 strains isolated from agricultural matrices. Seven E. coli O157:H7 isolates from different agricultural matrices—soil, compost, irrigation water, and sheep manure—were selected, and two ATCC strains were used as controls. The E. coli O157:H7 isolates were exposed to heat stress (56°C in 0.1% peptone water for up to 1 h) and starvation (in phosphate-buffered saline at 37°C for 15 days), and their survival was examined. GInaFiT freeware tool was used to perform regression analyses of the surviving populations. The Weibull model was identified as the most appropriate model for response of the isolates to heat stress, whereas the biphasic survival curves during starvation were fitted using the double Weibull model, indicating the adaptation to starvation or a resistant subpopulation. The inactivation time during heating to achieve the first decimal reduction time (δ) calculated with the Weibull parameters was the highest (45 min) for a compost isolate (Comp60A) and the lowest (28 min) for ATCC strain 43895. Two of the nine isolates (ATCC 43895 and a manure isolate) had β < 1, indicating that surviving populations adapted to heat stress, and six strains demonstrated downward concavity (β > 1), indicating decreasing heat resistance over time. The ATCC strains displayed the longest δ2 (>1,250 h) in response to starvation stress, compared with from 328 to 812 h for the environmental strains. The considerable variation in inactivation kinetics of E. coli O157:H7 highlights the importance of evaluating response to stress conditions among individual strains of a specific pathogen. Environmental isolates did not exhibit more robust response to stress conditions in this study compared with ATCC strains.

scholarly journals Regulation of Yeast-to-Hyphae Transition inYarrowia lipolytica

mSphere ◽  
2018 ◽  
Vol 3 (6) ◽  
Author(s):  
Kyle R. Pomraning ◽  
Erin L. Bredeweg ◽  
Eduard J. Kerkhoven ◽  
Kerrie Barry ◽  
Sajeet Haridas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Stress Response ◽  
Hyphal Growth ◽  
Genetic Screen ◽  
Morphological Transition ◽  
Histidine Kinases ◽  
Content Type ◽  
Forward Genetic Screen ◽  
Response To Stress

ABSTRACTThe yeastYarrowia lipolyticaundergoes a morphological transition from yeast-to-hyphal growth in response to environmental conditions. A forward genetic screen was used to identify mutants that reliably remain in the yeast phase, which were then assessed by whole-genome sequencing. All thesmoothmutants identified, so named because of their colony morphology, exhibit independent loss of DNA at a repetitive locus made up of interspersed ribosomal DNA and short 10- to 40-mer telomere-like repeats. The loss of repetitive DNA is associated with downregulation of genes with stress response elements (5′-CCCCT-3′) and upregulation of genes with cell cycle box (5′-ACGCG-3′) motifs in their promoter region. The stress response element is bound by the transcription factor Msn2p inSaccharomyces cerevisiae. We confirmed that theY. lipolyticamsn2(Ylmsn2) ortholog is required for hyphal growth and found that overexpression of Ylmsn2enables hyphal growth insmoothstrains. The cell cycle box is bound by the Mbp1p/Swi6p complex inS. cerevisiaeto regulate G1-to-S phase progression. We found that overexpression of either the Ylmbp1or Ylswi6homologs decreased hyphal growth and that deletion of either Ylmbp1or Ylswi6promotes hyphal growth insmoothstrains. A second forward genetic screen for reversion to hyphal growth was performed with thesmooth-33mutant to identify additional genetic factors regulating hyphal growth inY. lipolytica. Thirteen of the mutants sequenced from this screen had coding mutations in five kinases, including the histidine kinases Ylchk1and Ylnik1and kinases of the high-osmolarity glycerol response (HOG) mitogen-activated protein (MAP) kinase cascade Ylssk2, Ylpbs2, and Ylhog1. Together, these results demonstrate thatY. lipolyticatransitions to hyphal growth in response to stress through multiple signaling pathways.IMPORTANCEMany yeasts undergo a morphological transition from yeast-to-hyphal growth in response to environmental conditions. We used forward and reverse genetic techniques to identify genes regulating this transition inYarrowia lipolytica. We confirmed that the transcription factor Ylmsn2is required for the transition to hyphal growth and found that signaling by the histidine kinases Ylchk1and Ylnik1as well as the MAP kinases of the HOG pathway (Ylssk2, Ylpbs2, and Ylhog1) regulates the transition to hyphal growth. These results suggest thatY. lipolyticatransitions to hyphal growth in response to stress through multiple kinase pathways. Intriguingly, we found that a repetitive portion of the genome containing telomere-like and rDNA repeats may be involved in the transition to hyphal growth, suggesting a link between this region and the general stress response.

scholarly journals Death and population dynamics affect mutation rate estimates and evolvability under stress in bacteria

2017 ◽  
Author(s):  
Antoine Frénoy ◽  
Sebastian Bonhoeffer
Keyword(s):  
Population Dynamics ◽  
Mutation Rate ◽  
Death Rate ◽  
Mutation Rates ◽  
Resistance Mutations ◽  
Bacterial Populations ◽  
Plasmid Segregation ◽  
Genome Wide ◽  
Response To Stress ◽  
Induced Mutagenesis

AbstractThe stress-induced mutagenesis paradigm postulates that in response to stress, bacteria increase their genome-wide mutation rate, in turn increasing the chances that a descendant is able to withstand the stress. This has implications for antibiotic treatment: exposure to sub-inhibitory doses of antibiotics has been reported to increase bacterial mutation rates, and thus probably the rate at which resistance mutations appear and lead to treatment failure.Measuring mutation rates under stress, however, is problematic, because existing methods assume there is no death. Yet sub-inhibitory stress levels may induce a substantial death rate. Death events need to be compensated by extra replication to reach a given population size, thus giving more opportunities to acquire mutations. We show that ignoring death leads to a systematic overestimation of mutation rates under stress.We developed a system using plasmid segregation to measure death and growth rates simultaneously in bacterial populations. We use it to replicate classical experiments reporting antibiotic-induced mutagenesis. We found that a substantial death rate occurs at the tested sub-inhibitory concentrations, and taking this death into account lowers and sometimes removes the signal for stress-induced mutagenesis. Moreover even when antibiotics increase mutation rate, sub-inhibitory treatments do not increase genetic diversity and evolvability, again because of effects of the antibiotics on population dynamics.Beside showing that population dynamic is a crucial but neglected parameter affecting evolvability, we provide better experimental and computational tools to study evolvability under stress, leading to a re-assessment of the magnitude and significance of the stress-induced mutagenesis paradigm.

The endocrine response to stress

2011 ◽  
pp. 287-294
Author(s):  
David E. Henley ◽  
Joey M. Kaye ◽  
Stafford L. Lightman
Keyword(s):  
Stress Response ◽  
Initial Exposure ◽  
Behavioural Responses ◽  
Physiological Processes ◽  
Psychological Stressors ◽  
Endocrine Stress Response ◽  
The Face ◽  
Response To Stress ◽  
Trauma Injury ◽  
As Stress

In the face of any threat or challenge, either real or perceived, an organism must mount a series of coordinated and specific hormonal, autonomic, immune, and behavioural responses that allow it to either escape or adapt (1–3). To be successful, the characteristics and intensity of the response must match that posed by the threat itself and should last no longer than is necessary. A response that is either inadequate or excessive in terms of its specificity, intensity or duration may result in one or more of a multitude of psychological or physical pathologies (2–5). This concept of threat and the organism’s response to it is frequently recognized and understood as ‘stress’ but is so diverse that it lacks a universally accepted definition (2) and thus is difficult to investigate or study (6). In the early 1900s, Walter Cannon introduced the concept of homoeostasis (4)—an ideal steady state for all physiological processes. Stress has been defined as the state where this ideal is threatened. More easily appreciated, however, are those factors, both intrinsic and extrinsic, which represent a challenge to homoeostasis (termed stressors) and the complex physiological, hormonal, and behavioural responses that occur to restore the balance, the stress response (1). The importance of endocrine systems in this stress response was emphasized by Hans Selye (7), who described the need for multiple, integrated systems to respond in a coordinated fashion following exposure to a particular stressor. Nonspecific activation of the hypothalamic–pituitary–adrenal (HPA) and sympatho-adrenomedullary (SAM) axes occurred following initial exposure to a noxious stimulus. Continued exposure to the same agent has been shown to have lasting and damaging effects on various endocrine, immune, and other systems, although recovery from this state was possible provided the stress was terminated (7). In addition to various noxious agents, numerous potential stressors exist including exertion, physical extremes, trauma, injury, and psychological stress. Indeed, psychological stressors are some of the most potent stimuli of the endocrine stress response particularly when they involve elements of novelty, uncertainty, and unpredictability. This has been highlighted by the observation that anticipating an event can be as potent an activator of the stress response as the event itself (7).

scholarly journals Maize ZmBES1/BZR1-5 Decreases ABA Sensitivity and Confers Tolerance to Osmotic Stress in Transgenic Arabidopsis

2020 ◽  
Vol 21 (3) ◽  
pp. 996 ◽  
Author(s):  
Fuai Sun ◽  
Haoqiang Yu ◽  
Jingtao Qu ◽  
Yang Cao ◽  
Lei Ding ◽  
...  
Keyword(s):  
Stress Response ◽  
Drought Tolerance ◽  
Osmotic Stress ◽  
Transgenic Arabidopsis ◽  
Salt And Drought Tolerance ◽  
Aba Sensitivity ◽  
E Box ◽  
Mda Content ◽  
Response To Stress ◽  
Stress Related Genes

The BRI1-EMS suppressor 1 (BES1)/brassinazole-resistant 1 (BZR1) transcription factors, key components in the brassinosteroid signaling pathway, play pivotal roles in plant growth and development. However, the function of BES1/BZR1 in crops during stress response remains poorly understood. In the present study, we characterized ZmBES1/BZR1-5 from maize, which was localized to the nucleus and was responsive to abscisic acid (ABA), salt and drought stresses. Heterologous expression of ZmBES1/BZR1-5 in transgenic Arabidopsis resulted in decreased ABA sensitivity, facilitated shoot growth and root development, and enhanced salt and drought tolerance with lower malondialdehyde (MDA) content and relative electrolyte leakage (REL) under osmotic stress. The RNA sequencing (RNA-seq) analysis revealed that 84 common differentially expressed genes (DEGs) were regulated by ZmBES1/BZR1-5 in transgenic Arabidopsis. Subsequently, gene ontology and KEGG pathway enrichment analyses showed that the DEGs were enriched in response to stress, secondary metabolism and metabolic pathways. Furthermore, 30 DEGs were assigned to stress response and possessed 2–15 E-box elements in their promoters, which could be potentially recognized and bound by ZmBES1/BZR1-5. Taken together, our results reveal that the ZmBES1/BZR1-5 transcription factor positively regulates salt and drought tolerance by binding to E-box to induce the expression of downstream stress-related genes. Therefore, our study contributes to the better understanding of BES1/BZR1 function in the stress response of plants.

scholarly journals Plasma Transcortin Influences Endocrine and Behavioral Stress Responses in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 649-659 ◽  
Author(s):  
Elodie M. Richard ◽  
Jean-Christophe Helbling ◽  
Claudine Tridon ◽  
Aline Desmedt ◽  
Amandine M. Minni ◽  
...  
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Learned Helplessness ◽  
Critical Role ◽  
Adaptive Responses ◽  
Adrenal Axis ◽  
Response To Stress ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Deficient Mice ◽  
Pituitary Adrenal Axis

Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on behaviors linked to anxiety and depression traits in animals. We show that CBG deficiency in mice results in markedly reduced total circulating corticosterone at rest and in response to stress. Interestingly, free corticosterone concentrations are normal at rest but present a reduced surge after stress in transcortin-deficient mice. No differences were detected between transcortin-deficient mice for anxiety-related traits. However, transcortin-deficient mice display increased immobility in the forced-swimming test and markedly enhanced learned helplessness after prolonged uncontrollable stress. The latter is associated with an approximately 30% decrease in circulating levels of free corticosterone as well as reduced Egr-1 mRNA expression in hippocampus in CBG-deficient mice. Additionally, transcortin-deficient mice show no sensitization to cocaine-induced locomotor responses, a well described corticosterone-dependent test. Thus, transcortin deficiency leads to insufficient glucocorticoid signaling and altered behavioral responses after stress. These findings uncover the critical role of plasma transcortin in providing an adequate endocrine and behavioral response to stress.

scholarly journals Systematically Altering Bacterial SOS Activity under Stress Reveals Therapeutic Strategies for Potentiating Antibiotics

mSphere ◽  
2016 ◽  
Vol 1 (4) ◽  
Author(s):  
Charlie Y. Mo ◽  
Sara A. Manning ◽  
Manuela Roggiani ◽  
Matthew J. Culyba ◽  
Amanda N. Samuels ◽  
...  
Keyword(s):  
Dna Damage ◽  
Drug Resistance ◽  
Stress Response ◽  
Antibiotic Treatment ◽  
Molecular Targets ◽  
Sos Response ◽  
Mutation Rates ◽  
Induced Mutation ◽  
Acquired Drug Resistance ◽  
Evolution Of Resistance

ABSTRACT Our antibiotic arsenal is becoming depleted, in part, because bacteria have the ability to rapidly adapt and acquire resistance to our best agents. The SOS pathway, a widely conserved DNA damage stress response in bacteria, is activated by many antibiotics and has been shown to play central role in promoting survival and the evolution of resistance under antibiotic stress. As a result, targeting the SOS response has been proposed as an adjuvant strategy to revitalize our current antibiotic arsenal. However, the optimal molecular targets and partner antibiotics for such an approach remain unclear. In this study, focusing on the two key regulators of the SOS response, LexA and RecA, we provide the first comprehensive assessment of how to target the SOS response in order to increase bacterial susceptibility and reduce mutagenesis under antibiotic treatment. The bacterial SOS response is a DNA damage repair network that is strongly implicated in both survival and acquired drug resistance under antimicrobial stress. The two SOS regulators, LexA and RecA, have therefore emerged as potential targets for adjuvant therapies aimed at combating resistance, although many open questions remain. For example, it is not well understood whether SOS hyperactivation is a viable therapeutic approach or whether LexA or RecA is a better target. Furthermore, it is important to determine which antimicrobials could serve as the best treatment partners with SOS-targeting adjuvants. Here we derived Escherichia coli strains that have mutations in either lexA or recA genes in order to cover the full spectrum of possible SOS activity levels. We then systematically analyzed a wide range of antimicrobials by comparing the mean inhibitory concentrations (MICs) and induced mutation rates for each drug-strain combination. We first show that significant changes in MICs are largely confined to DNA-damaging antibiotics, with strains containing a constitutively repressed SOS response impacted to a greater extent than hyperactivated strains. Second, antibiotic-induced mutation rates were suppressed when SOS activity was reduced, and this trend was observed across a wider spectrum of antibiotics. Finally, perturbing either LexA or RecA proved to be equally viable strategies for targeting the SOS response. Our work provides support for multiple adjuvant strategies, while also suggesting that the combination of an SOS inhibitor with a DNA-damaging antibiotic could offer the best potential for lowering MICs and decreasing acquired drug resistance. IMPORTANCE Our antibiotic arsenal is becoming depleted, in part, because bacteria have the ability to rapidly adapt and acquire resistance to our best agents. The SOS pathway, a widely conserved DNA damage stress response in bacteria, is activated by many antibiotics and has been shown to play central role in promoting survival and the evolution of resistance under antibiotic stress. As a result, targeting the SOS response has been proposed as an adjuvant strategy to revitalize our current antibiotic arsenal. However, the optimal molecular targets and partner antibiotics for such an approach remain unclear. In this study, focusing on the two key regulators of the SOS response, LexA and RecA, we provide the first comprehensive assessment of how to target the SOS response in order to increase bacterial susceptibility and reduce mutagenesis under antibiotic treatment.

scholarly journals The unpredictability of prolonged activation of stress response pathways

2015 ◽  
Vol 209 (6) ◽  
pp. 781-787 ◽  
Author(s):  
Lilian T. Lamech ◽  
Cole M. Haynes
Keyword(s):  
Stress Response ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Degenerative Diseases ◽  
Response To Stress ◽  
Cellular Compartments

In response to stress, cellular compartments activate signaling pathways that mediate transcriptional programs to promote survival and reestablish homeostasis. Manipulation of the magnitude and duration of the activation of stress responses has been proposed as a strategy to prevent or repair the damage associated with aging or degenerative diseases. However, as these pathways likely evolved to respond specifically to transient perturbations, the unpredictability of prolonged activation should be considered.

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