scholarly journals The effect of chronic and acute stressors, and their interaction, on gonadal function: an experimental test during gonadal recrudescence

2017 ◽  
Author(s):  
Mikus Abolins-Abols ◽  
Rachel E. Hanauer ◽  
Kimberly A. Rosvall ◽  
Mark P. Peterson ◽  
Ellen D. Ketterson
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Cellular Stress Response ◽  
Gonadal Function ◽  
Transcriptomic Response ◽  
Stress Changes ◽  
Chronic Disturbance ◽  
Gonadal Recrudescence ◽  
Acute Stressor

AbstractOrganisms are expected to invest less in reproduction in response to a stressor, but theory predicts that this effect should depend on the frequency of stressors in the environment. Here we investigated how an acute stressor affected gonadal function in a songbird, and how long-term differences in the stress environment influenced these acute stress responses. We exposed male Dark-eyed Juncos (Junco hyemalis) either to chronic or minimal (control) disturbance during gonadal recrudescence, after which we measured baseline testosterone, testosterone after an acute handling stressor, and the ability to elevate testosterone in response to hormonal stimulation. In a 2x2 design, we then euthanized males from the two chronic treatment groups either immediately or after an acute stressor to investigate the effect of these treatments on the gonadal transcriptome. We found that chronically disturbed birds had marginally lower testosterone. The acute stressor suppressed testosterone in control birds, but not in the chronic disturbance group. The ability to elevate testosterone did not differ between the chronic treatments. Surprisingly, chronic disturbance had a weak effect on the testicular transcriptome, and did not affect transcriptomic response to the acute stressor. The acute stressor, on the other hand, upregulated cellular stress response, and affected expression of genes associated with hormonal stress-response. Overall, we show that both chronic and acute stressors affect reproductive function, and that chronic stress changes how acute stressors affect testosterone physiology. Our findings also suggest that acute and chronic stressors affect testes differently, and that gonadal function is relatively robust to long-term stressors.Summary statementAn acute stressor downregulated testosterone production, but this effect was absent in chronically disturbed birds. The acute stressor had a strong effect on the gonadal transcriptome, whereas chronic disturbance had a negligible effect.

scholarly journals Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 99
Author(s):  
Shweta Devi ◽  
Vijay Kumar ◽  
Sandeep Kumar Singh ◽  
Ashish Kant Dubey ◽  
Jong-Joo Kim
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Neurodegenerative Disorders ◽  
Cell Damage ◽  
Cellular Stress ◽  
Clinical Manifestations ◽  
Cellular Stress Response ◽  
Dramatic Rise ◽  
Cellular Stress Responses

Neurodegenerative disorders, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), are the most concerning disorders due to the lack of effective therapy and dramatic rise in affected cases. Although these disorders have diverse clinical manifestations, they all share a common cellular stress response. These cellular stress responses including neuroinflammation, oxidative stress, proteotoxicity, and endoplasmic reticulum (ER)-stress, which combats with stress conditions. Environmental stress/toxicity weakened the cellular stress response which results in cell damage. Small molecules, such as flavonoids, could reduce cellular stress and have gained much attention in recent years. Evidence has shown the potential use of flavonoids in several ways, such as antioxidants, anti-inflammatory, and anti-apoptotic, yet their mechanism is still elusive. This review provides an insight into the potential role of flavonoids against cellular stress response that prevent the pathogenesis of neurodegenerative disorders.

scholarly journals Environmental Conditions Modulate the Transcriptomic Response of Both Caulobacter crescentus Morphotypes to Cu Stress

2021 ◽  
Vol 9 (6) ◽  
pp. 1116
Author(s):  
Laurens Maertens ◽  
Pauline Cherry ◽  
Françoise Tilquin ◽  
Rob Van Houdt ◽  
Jean-Yves Matroule
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Stress Responses ◽  
Caulobacter Crescentus ◽  
Oxidative Stress Response ◽  
Transport Systems ◽  
Transcriptomic Response ◽  
Swarmer Cell ◽  
Cu Stress ◽  
Cellular Environment

Bacteria encounter elevated copper (Cu) concentrations in multiple environments, varying from mining wastes to antimicrobial applications of copper. As the role of the environment in the bacterial response to Cu ion exposure remains elusive, we used a tagRNA-seq approach to elucidate the disparate responses of two morphotypes of Caulobacter crescentus NA1000 to moderate Cu stress in a complex rich (PYE) medium and a defined poor (M2G) medium. The transcriptome was more responsive in M2G, where we observed an extensive oxidative stress response and reconfiguration of the proteome, as well as the induction of metal resistance clusters. In PYE, little evidence was found for an oxidative stress response, but several transport systems were differentially expressed, and an increased need for histidine was apparent. These results show that the Cu stress response is strongly dependent on the cellular environment. In addition, induction of the extracytoplasmic function sigma factor SigF and its regulon was shared by the Cu stress responses in both media, and its central role was confirmed by the phenotypic screening of a sigF::Tn5 mutant. In both media, stalked cells were more responsive to Cu stress than swarmer cells, and a stronger basal expression of several cell protection systems was noted, indicating that the swarmer cell is inherently more Cu resistant. Our approach also allowed for detecting several new transcription start sites, putatively indicating small regulatory RNAs, and additional levels of Cu-responsive regulation.

scholarly journals Short- and Long-Term Transcriptomic Responses of Escherichia coli to Biocides: a Systems Analysis

2020 ◽  
Vol 86 (14) ◽  
Author(s):  
Beatriz Merchel Piovesan Pereira ◽  
Xiaokang Wang ◽  
Ilias Tagkopoulos
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Stress Responses ◽  
Zinc Homeostasis ◽  
Cross Resistance ◽  
Transcriptional Responses ◽  
Systematic Analysis ◽  
Content Type ◽  
Short Term Exposure

ABSTRACT The mechanisms of the bacterial response to biocides are poorly understood, despite their broad application. To identify the genetic basis and pathways implicated in the biocide stress response, we exposed Escherichia coli populations to 10 ubiquitous biocides. By comparing the transcriptional responses between a short-term exposure (30 min) and a long-term exposure (8 to 12 h) to biocide stress, we established the common gene and pathway clusters that are implicated in general and biocide-specific stress responses. Our analysis revealed a temporal choreography, starting from the upregulation of chaperones to the subsequent repression of motility and chemotaxis pathways and the induction of an anaerobic pool of enzymes and biofilm regulators. A systematic analysis of the transcriptional data identified a zur-regulated gene cluster to be highly active in the stress response against sodium hypochlorite and peracetic acid, presenting a link between the biocide stress response and zinc homeostasis. Susceptibility assays with knockout mutants further validated our findings and provide clear targets for downstream investigation of the implicated mechanisms of action. IMPORTANCE Antiseptics and disinfectant products are of great importance to control and eliminate pathogens, especially in settings such as hospitals and the food industry. Such products are widely distributed and frequently poorly regulated. Occasional outbreaks have been associated with microbes resistant to such compounds, and researchers have indicated potential cross-resistance with antibiotics. Despite that, there are many gaps in knowledge about the bacterial stress response and the mechanisms of microbial resistance to antiseptics and disinfectants. We investigated the stress response of the bacterium Escherichia coli to 10 common disinfectant and antiseptic chemicals to shed light on the potential mechanisms of tolerance to such compounds.

scholarly journals Stressors and Stress Responses in Cystic Fibrosis

2018 ◽  
Vol 5 (1) ◽  
pp. 11-29 ◽  
Author(s):  
Zsuzsa Bebok ◽  
Lianwu Fu
Keyword(s):  
Cystic Fibrosis ◽  
Stress Response ◽  
Stress Responses ◽  
Genetic Disorder ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
Bicarbonate Transport ◽  
Persistent Infections ◽  
Human Disorders ◽  
The Unfolded Protein Response

Abstract Cystic fibrosis (CF) is a life-shortening, genetic disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR). The primary cause of CF is reduced CFTR-mediated chloride and bicarbonate transport, due to mutations in CFTR. However, inflammation and persistent infections influence clinical outcome. Cellular stress response pathways, such as the unfolded protein response (UPR) and the integrated stress response (ISR), referred to here as cellular stress response pathways (SRPs), contribute to the pathology of human disorders. Multiple studies have indicated activation of SRPs in CF tissues. We review our present understanding of how SRPs are activated in CF and their contribution to pathology. We conclude that reduced CFTR function in CF organs establishes a tissue environment in which internal or external insults activate SRPs. SRPs contribute to CF pathogenesis by reducing CFTR expression, enhancing inflammation with consequent tissue remodeling. Understanding the contribution of SRPs to CF pathogenesis is crucial even in the era of CFTR “modulators” that are designed to potentiate, correct or amplify CFTR function, since there is an urgent need for supportive treatments. Importantly, CF patients with established pathology could benefit from the targeted use of drugs that modulate SRPs to reduce the symptoms.

Effects of culling on vigilance behaviour and endogenous stress response of female fallow deer

2016 ◽  
Vol 43 (3) ◽  
pp. 189 ◽  
Author(s):  
I. Pecorella ◽  
F. Ferretti ◽  
A. Sforzi ◽  
E. Macchi
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Mediterranean Area ◽  
Fallow Deer ◽  
Wild Ungulates ◽  
Dama Dama ◽  
Vigilance Behaviour ◽  
Faecal Samples ◽  
Predator Behaviour

Context Human activities can induce behavioural and stress responses in wild animals. Information is scarce on the effects of culling on anti-predator behaviour and endogenous stress response of wild ungulates. Aims In a Mediterranean area, we evaluated the effects of culling on vigilance, foraging and endogenous stress response of female fallow deer (Dama dama). Methods Effects of culling were evaluated through behavioural observations and hormone analyses of faecal samples. Key results In an area where culling occurred (C), individuals showed significantly greater vigilance rates and foraged closer to wood than in an area with no culling (NC). In C, 24 h after culling, faecal cortisol concentrations were greater than those recorded in NC, but they decreased significantly to values comparable to (48 h post-shot) and lower than (72 h post-shot) those observed in NC. Conclusions Most likely, culling determined behavioural responses in female fallow deer, but did not trigger long-term physiological effects. Implications Increased anti-predator behaviour may complicate the implementation of long-term culling programs.

scholarly journals Reovirus Induces and Benefits from an Integrated Cellular Stress Response

2006 ◽  
Vol 80 (4) ◽  
pp. 2019-2033 ◽  
Author(s):  
Jennifer A. Smith ◽  
Stephen C. Schmechel ◽  
Arvind Raghavan ◽  
Michelle Abelson ◽  
Cavan Reilly ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stress Response ◽  
Stress Responses ◽  
Cellular Stress Response ◽  
Initiation Factor ◽  
Viral Protein Synthesis ◽  
Protein Levels ◽  
Eif2α Phosphorylation ◽  
Infected Cells ◽  
Reovirus Replication

ABSTRACT Following infection with most reovirus strains, viral protein synthesis is robust, even when cellular translation is inhibited. To gain further insight into pathways that regulate translation in reovirus-infected cells, we performed a comparative microarray analysis of cellular gene expression following infection with two strains of reovirus that inhibit host translation (clone 8 and clone 87) and one strain that does not (Dearing). Infection with clone 8 and clone 87 significantly increased the expression of cellular genes characteristic of stress responses, including the integrated stress response. Infection with these same strains decreased transcript and protein levels of P58IPK, the cellular inhibitor of the eukaryotic initiation factor 2α (eIF2α) kinases PKR and PERK. Since infection with host shutoff-inducing strains of reovirus impacted cellular pathways that control eIF2α phosphorylation and unphosphorylated eIF2α is required for translation initiation, we examined reovirus replication in a variety of cell lines with mutations that impact eIF2α phosphorylation. Our results revealed that reovirus replication is more efficient in the presence of eIF2α kinases and phosphorylatable eIF2α. When eIF2α is phosphorylated, it promotes the synthesis of ATF4, a transcription factor that controls cellular recovery from stress. We found that the presence of this transcription factor increased reovirus yields 10- to 100-fold. eIF2α phosphorylation also led to the formation of stress granules in reovirus-infected cells. Based on these results, we hypothesize that eIF2α phosphorylation facilitates reovirus replication in two ways—first, by inducing ATF4 synthesis, and second, by creating an environment that places abundant reovirus transcripts at a competitive advantage for limited translational components.

scholarly journals A combined lifestyle intervention induces a sensitization of the blood transcriptomic response to a nutrient challenge

2021 ◽  
Author(s):  
Thies Gehrmann ◽  
Marian Beekman ◽  
Joris Deelen ◽  
Linda Partridge ◽  
Ondine van de Rest ◽  
...  
Keyword(s):  
Stress Response ◽  
Lifestyle Intervention ◽  
The Elderly ◽  
Cellular Stress Response ◽  
Lifestyle Interventions ◽  
Phenotypic Flexibility ◽  
Transcriptomic Response ◽  
Healthy Elderly ◽  
Fasted State ◽  
Novel Biomarkers

The global population is growing older. As age is a primary risk factor of (multi)morbidity, there is a need for novel indicators to predict, track, treat and prevent the development of disease. Lifestyle interventions have shown promising results in improving the health of participants and reducing the risk for disease, but in the elderly population, such interventions often show less reliable or subtle effects on health outcomes. This is further complicated by a poor understanding of the homeodynamics and the molecular effects of lifestyle interventions, by which their effects of a lifestyle intervention remain obscured. In the Growing Old Together (GOTO) study, we examined the responses of 164 healthy, elderly men and women to a 13-week combined physical and dietary lifestyle intervention. In addition to collecting blood samples at a fasted state, we sampled blood also 30 minutes following a standardized meal. This allows us to investigate an intervention response not only in the traditional fasted state, but also in the blood metabolic and cellular responses to a nutrient challenge. We investigated the transcriptomic and metabolomic responses to this nutrient challenge, how these responses relate to each other, and how this response is affected by the lifestyle intervention. We find that the intervention has very little effect on the fasted blood transcriptome, but that the nutrient challenge induces a large translational inhibition, and an innate immune activation, which together comprise a cellular stress response that is stimulated by the intervention. A sex-specific analysis reveals that although the same set of genes respond in the same direction in both males and females, the magnitude of these effects differ, and are modulated differently by the intervention. On the other hand, the metabolomic response to the nutrient challenge is largely unaffected by the intervention, and the correlation between the metabolomic nutrient response and transcriptomic modules indicates that the change in transcriptomic response to the nutrient challenge is independent from a change in cellular metabolomic environment. This work constitutes a glance at the acute transcriptomic stress response to nutrient intake in blood, and how a lifestyle intervention affects this response in healthy elderly, and may lead to the development of novel biomarkers to capture the phenotypic flexibility of health.

scholarly journals Deciphering the genetic and transcriptional basis of cross-stress responses in Escherichia coli under complex evolutionary scenarios

2014 ◽  
Author(s):  
Violeta Zorraquino-Salvo ◽  
Semarhy Quinones-Soto ◽  
Minseung Kim ◽  
Navneet Rai ◽  
Ilias Tagkopoulos
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Stress Responses ◽  
Metal Ion ◽  
Cellular Stress Response ◽  
Metal Ion Binding ◽  
Evolutionary Potential ◽  
Specific Expression ◽  
Stress Vulnerability ◽  
Stress Protection

A tantalizing question in microbial physiology is the inter-dependence and evolutionary potential of cellular stress response across multiple environmental dimensions. To address this question, we comprehensively characterized the cross-stress behavior of wild-type and evolved Escherichia coli populations in five abiotic stresses (n-butanol, osmotic, alkaline, acidic, and oxidative) by performing genome-scale genetic, transcriptional and growth profiling, thus identifying 18 cases of cross-stress protection and one case of cross-stress vulnerability. We identified 18 cases of cross-stress protection and one case of cross-stress vulnerability, along with core and stress-specific networks. We tested several hypotheses regarding the effect of the stress order, stress combinations, mutation reversal and varying environments to the evolution and final cellular fitness of the respective populations. Our results argue of a common systems-level core of the stress response with several crucial implicated pathways that include metal ion binding and glycolysis/gluconeogenesis that is further complemented by a stress-specific expression program.

scholarly journals Effect of Combined Stressors on C. elegans Lifespan

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 667-667
Author(s):  
Bradford Hull ◽  
George Sutphin
Keyword(s):  
Heavy Metal ◽  
Stress Response ◽  
Stress Responses ◽  
Cellular Response ◽  
Multiple Stressors ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
C Elegans ◽  
Arsenic Copper ◽  
The Impact

Abstract Cellular stress is a fundamental component of age-associated disease. Cells experience many forms of stress (oxidative, heavy metal, etc.), and as we age the burden of stress and resulting damage increases while our cells’ ability to deal with the consequences becomes diminished due to dysregulation of cellular stress response pathways. By understanding how cells respond to stress we aim to slow age-associated deterioration and develop treatment targets for age-associated disease. The majority of past work has focused on understanding responses to individual stressors. In contrast, how pathology and stress responses differ in the presence of multiple stressors is relatively unknown; we investigate that here. We cultured worms on agar plates with different combinations of arsenic, copper, and DTT (which create oxidative/proteotoxic, heavy metal, and endoplasmic reticulum (ER) stress, respectively) at doses that result in 20% lifespan reduction individually and measured the effect on lifespan. We found that arsenic/copper and arsenic/DTT combinations created additive lifespan reductions while the copper/DTT combination created an antagonistic lifespan reduction when compared to controls (p<0.05). This antagonistic toxicity suggests an interaction either between the mechanisms of toxicity or the cellular response to copper and DTT. We are now evaluating the impact of copper and DTT individually and in combination on unfolded protein and heavy metal response pathways to understand the underlying mechanism of the interaction. Additionally, we are continuing to screen stressors to identify combinations that cause non-additive (synergistic or antagonistic) toxicity to build a comprehensive model of the genetic stress response network in C. elegans.

scholarly journals Redefining proteostasis transcription factors in organismal stress responses, development, metabolism, and health

2020 ◽  
Vol 401 (9) ◽  
pp. 1005-1018
Author(s):  
Laura M. Jones ◽  
Yannic Chen ◽  
Patricija van Oosten-Hawle
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Stress Response ◽  
Stress Responses ◽  
Stress Condition ◽  
Physiological Responses ◽  
Defense Responses ◽  
Cellular Stress Response ◽  
Proteotoxic Stress ◽  
Eukaryotic Organisms

AbstractEukaryotic organisms have evolved complex and robust cellular stress response pathways to ensure maintenance of proteostasis and survival during fluctuating environmental conditions. Highly conserved stress response pathways can be triggered and coordinated at the cell-autonomous and cell-nonautonomous level by proteostasis transcription factors, including HSF1, SKN-1/NRF2, HIF1, and DAF-16/FOXO that combat proteotoxic stress caused by environmental challenges. While these transcription factors are often associated with a specific stress condition, they also direct “noncanonical” transcriptional programs that serve to integrate a multitude of physiological responses required for development, metabolism, and defense responses to pathogen infections. In this review, we outline the established function of these key proteostasis transcription factors at the cell-autonomous and cell-nonautonomous level and discuss a newly emerging stress responsive transcription factor, PQM-1, within the proteostasis network. We look beyond the canonical stress response roles of proteostasis transcription factors and highlight their function in integrating different physiological stimuli to maintain cytosolic organismal proteostasis.

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