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.

N6-methyladenosine modification modulate in the heat stress of sheep (Ovis aries)

2019 ◽  
Author(s):  
Zengkui Lu ◽  
Huihua Wang ◽  
Youji Ma ◽  
Mingxing Chu ◽  
Kai Quan ◽  
...  
Keyword(s):  
Heat Stress ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Large Scale ◽  
Ovis Aries ◽  
Stop Codons ◽  
Coding Regions ◽  
Mrna Methylation ◽  
Response To Stress ◽  
And Control

Abstract Background: Intensive and large-scale development of the sheep industry and increases in global temperature are increasingly exposing sheep to heat stress. N6-methyladenosine (m6A) mRNA methylation varies in response to stress, and can link external stress with complex transcriptional and post-transcriptional processes. However, no m6A mRNA methylation map has been obtained for sheep, nor is it known what effect this has on regulating heat stress in sheep. Results: A total of 8,306 and 12,958 m6A peaks were detected in heat stress and control groups, respectively, with 2,697 and 5,494 genes associated with each. Peaks were mainly enriched in coding regions and near stop codons with classical RRACH motifs. Methylation levels of heat stress and control sheep were higher near stop codons, although methylation was significantly lower in heat stress sheep. GO revealed that differential m6A-containing genes were mainly enriched in the nucleus and were involved in several stress responses and substance metabolism processes. KEGG pathway analysis found that differential m6A-containing genes were significantly enriched in Rap1, FoxO, MAPK, and other signaling pathways of the stress response, and TGF-beta, AMPK, Wnt, and other signaling pathways involved in fat metabolism. These m6A-modified genes were moderately expressed in both heat stress and control sheep, and the enrichment of m6A modification was significantly negatively correlated with gene expression. Conclusions: Our results showed that m6A mRNA methylation modifications regulate heat stress in sheep, and it also provided a new way for the study of animal response to heat stress.

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 Ahi1 regulates the nuclear translocation of glucocorticoid receptor to modulate stress response

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Wang ◽  
Ning Xin ◽  
Xuanchen Qian ◽  
Lijing Zhai ◽  
Zhigang Miao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Stress Responses ◽  
Glucocorticoid Receptors ◽  
Stress Condition ◽  
Nuclear Translocation ◽  
Therapeutic Effects ◽  
Important Regulator ◽  
Response To Stress ◽  
Stressed Cells

AbstractStress activates the nuclear translocation of glucocorticoid receptors (GR) to trigger gene expression. Abnormal GR levels can alter the stress responses in animals and therapeutic effects of antidepressants. Here, we reported that stress-mediated nuclear translocation of GR reduced Ahi1 in the stressed cells and mouse brains. Ahi1 interacts with GR to stabilize each other in the cytoplasm. Importantly, Ahi1 deficiency promotes the degradation of GR in the cytoplasm and reduced the nuclear translocation of GR in response to stress. Genetic depletion of Ahi1 in mice caused hyposensitivity to antidepressants under the stress condition. These findings suggest that AHI1 is an important regulator of GR level and may serve as a therapeutic target for stress-related disorders.

scholarly journals Histone H3 threonine 11 phosphorylation by Sch9 and CK2 regulates chronological lifespan by controlling the nutritional stress response

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Seunghee Oh ◽  
Tamaki Suganuma ◽  
Madelaine M Gogol ◽  
Jerry L Workman
Keyword(s):  
Stress Response ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Histone H3 ◽  
Nutritional Stress ◽  
Stress Conditions ◽  
Metabolic Status ◽  
Chronological Lifespan ◽  
Nutrient Signaling ◽  
Altered Metabolism

Upon nutritional stress, the metabolic status of cells is changed by nutrient signaling pathways to ensure survival. Altered metabolism by nutrient signaling pathways has been suggested to influence cellular lifespan. However, it remains unclear how chromatin regulation is involved in this process. Here, we found that histone H3 threonine 11 phosphorylation (H3pT11) functions as a marker for nutritional stress and aging. Sch9 and CK2 kinases cooperatively regulate H3pT11 under stress conditions. Importantly, H3pT11 defective mutants prolonged chronological lifespan (CLS) by altering nutritional stress responses. Thus, the phosphorylation of H3T11 by Sch9 and CK2 links a nutritional stress response to chromatin in the regulation of CLS.

scholarly journals Histone H3 T11 phosphorylation by Sch9 and CK2 regulates lifespan by controlling the nutritional stress response

2018 ◽  
Author(s):  
Seunghee Oh ◽  
Tamaki Suganuma ◽  
Madelaine M. Gogol ◽  
Jerry L. Workman
Keyword(s):  
Stress Response ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Histone H3 ◽  
Nutritional Stress ◽  
Stress Conditions ◽  
Metabolic Status ◽  
Chromatin Regulation ◽  
Nutrient Signaling ◽  
Altered Metabolism

AbstractUpon nutritional stress, the metabolic status of cells is changed by nutrient signaling pathways to ensure survival. Altered metabolism by nutrient signaling pathways has been suggested to influence cellular lifespan. However, it remains unclear how chromatin regulation is involved in this process. Here, we found that histone H3 threonine 11 phosphorylation (H3pT11) functions as a marker for nutritional stress and aging. Sch9 and CK2 kinases cooperatively regulate H3pT11 under stress conditions. Importantly, H3pT11 defective mutants prolonged chronological lifespan by altering nutritional stress responses. Thus, the phosphorylation of H3T11 by Sch9 and CK2 engages a nutritional stress response to chromatin in the regulation of lifespan.

scholarly journals A Conserved Stress-activated Protein Kinase Regulates a Core Stress Response in the Human PathogenCandida albicans

2004 ◽  
Vol 15 (9) ◽  
pp. 4179-4190 ◽  
Author(s):  
Deborah A. Smith ◽  
Susan Nicholls ◽  
Brian A. Morgan ◽  
Alistair J.P. Brown ◽  
Janet Quinn
Keyword(s):  
Stress Response ◽  
Protein Kinase ◽  
Stress Responses ◽  
Stress Conditions ◽  
Human Pathogen ◽  
Environmental Niche ◽  
The Core ◽  
Response To Stress ◽  
Molecular Circuitry

Previous work has implicated the Hog1 stress-activated protein kinase (SAPK) in osmotic and oxidative stress responses in the human pathogen Candida albicans. In this study, we have characterized the role of Hog1 in mediating these and other stress responses in C. albicans. We provide evidence that a SAPK-dependent core stress response exists in this pathogen. The Hog1 SAPK is phosphorylated and it accumulates in the nucleus in response to diverse stress conditions. In addition, we have identified Hog1-regulated genes that are induced in response to stress conditions that activate Hog1. These analyses reveal both activator and repressor functions for the Hog1 SAPK. Our results also demonstrate that stress cross-protection, a classical hallmark of the core stress response, occurs in C. albicans between stresses that activate the Hog1 SAPK. Importantly, we find that the core stress response in C. albicans has adapted to the environmental niche of this human pathogen. This niche specificity is reflected by the specific environmental conditions that drive the Hog1-regulated core stress response in C. albicans and by differences in the molecular circuitry that control this response.

scholarly journals The epigenetic regulator G9a attenuates stress-induced resistance and metabolic transcriptional programs across different stressors and species

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Human Riahi ◽  
Michaela Fenckova ◽  
Kayla J. Goruk ◽  
Annette Schenck ◽  
Jamie M. Kramer
Keyword(s):  
Stress Response ◽  
Signaling Pathways ◽  
Resistance Genes ◽  
Stress Responses ◽  
Stress Resistance ◽  
Transcriptional Activation ◽  
Infectious Agent ◽  
Metabolic Homeostasis ◽  
Resistance Factors ◽  
Stress Dependent

Abstract Background Resistance and tolerance are two coexisting defense strategies for fighting infections. Resistance is mediated by signaling pathways that induce transcriptional activation of resistance factors that directly eliminate the pathogen. Tolerance refers to adaptations that limit the health impact of a given pathogen burden, without targeting the infectious agent. The key players governing immune tolerance are largely unknown. In Drosophila, the histone H3 lysine 9 (H3K9) methyltransferase G9a was shown to mediate tolerance to virus infection and oxidative stress (OS), suggesting that abiotic stresses like OS may also evoke tolerance mechanisms. In response to both virus and OS, stress resistance genes were overinduced in Drosophila G9a mutants, suggesting an intact but overactive stress response. We recently demonstrated that G9a promotes tolerance to OS by maintaining metabolic homeostasis and safeguarding energy availability, but it remained unclear if this mechanism also applies to viral infection, or is conserved in other species and stress responses. To address these questions, we analyzed publicly available datasets from Drosophila, mouse, and human in which global gene expression levels were measured in G9a-depleted conditions and controls at different time points upon stress exposure. Results In all investigated datasets, G9a attenuates the transcriptional stress responses that confer resistance against the encountered stressor. Comparative analysis of conserved G9a-dependent stress response genes suggests that G9a is an intimate part of the design principles of stress resistance, buffering the induction of promiscuous stress signaling pathways and stress-specific resistance factors. Importantly, we find stress-dependent downregulation of metabolic genes to also be dependent on G9a across all of the tested datasets. Conclusions These results suggest that G9a sets the balance between activation of resistance genes and maintaining metabolic homeostasis, thereby ensuring optimal organismal performance during exposure to diverse types of stress across different species. We therefore propose G9a as a potentially conserved master regulator underlying the widely important, yet poorly understood, concept of stress tolerance.

scholarly journals Genome-Wide Identification of the B-BOX Genes that Respond to Multiple Ripening Related Signals in Sweet Cherry Fruit

2021 ◽  
Vol 22 (4) ◽  
pp. 1622
Author(s):  
Yanyan Wang ◽  
Zefeng Zhai ◽  
Yueting Sun ◽  
Chen Feng ◽  
Xiang Peng ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Stress Responses ◽  
Fruit Development ◽  
Sweet Cherry ◽  
Anthocyanin Biosynthesis ◽  
Expression Patterns ◽  
Light Induction ◽  
Promoter Regions ◽  
Genome Database ◽  
Gene Structures

B-BOX proteins are zinc finger transcription factors that play important roles in plant growth, development, and abiotic stress responses. In this study, we identified 15 PavBBX genes in the genome database of sweet cherry. We systematically analyzed the gene structures, clustering characteristics, and expression patterns of these genes during fruit development and in response to light and various hormones. The PavBBX genes were divided into five subgroups. The promoter regions of the PavBBX genes contain cis-acting elements related to plant development, hormones, and stress. qRT-PCR revealed five upregulated and eight downregulated PavBBX genes during fruit development. In addition, PavBBX6, PavBBX9, and PavBBX11 were upregulated in response to light induction. We also found that ABA, BR, and GA3 contents significantly increased in response to light induction. Furthermore, the expression of several PavBBX genes was highly correlated with the expression of anthocyanin biosynthesis genes, light-responsive genes, and genes that function in multiple hormone signaling pathways. Some PavBBX genes were strongly induced by ABA, GA, and BR treatment. Notably, PavBBX6 and PavBBX9 responded to all three hormones. Taken together, BBX proteins likely play major roles in regulating anthocyanin biosynthesis in sweet cherry fruit by integrating light, ABA, GA, and BR signaling pathways.

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.

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