Stress hormone dynamics: an adaptation to migration?

The hormone corticosterone (CORT) is an important component of a bird’s response to environmental stress, but it can also have negative effects. Therefore, birds on migration are hypothesized to have repressed stress responses (migration-modulation hypothesis). In contrast to earlier studies on long-distance migrants, we evaluate this hypothesis in a population containing both migratory and resident individuals. We use a population of partially migratory blue tits ( Cyanistes caeruleus ) in southern Sweden as a model species. Migrants had higher CORT levels at the time of capture than residents, indicating migratory preparations, adaptation to stressors, higher allostatic load or possibly low social status. Migrants and residents had the same stress response, thus contradicting the migration-modulation hypothesis. We suggest that migrants travelling short distances are more benefited than harmed by retaining the ability to respond to stress.

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Ribosomal stress-surveillance: three pathways is a magic number

Nucleic Acids Research ◽

10.1093/nar/gkaa757 ◽

2020 ◽

Vol 48 (19) ◽

pp. 10648-10661 ◽

Cited By ~ 2

Author(s):

Anna Constance Vind ◽

Aitana Victoria Genzor ◽

Simon Bekker-Jensen

Keyword(s):

Stress Response ◽

Stress Responses ◽

Map Kinases ◽

Cell Function ◽

Therapeutic Potential ◽

Magic Number ◽

Physiological Role ◽

Negative Effects ◽

Mitogen Activated Protein ◽

Activation Mechanisms

Abstract Cells rely on stress response pathways to uphold cellular homeostasis and limit the negative effects of harmful environmental stimuli. The stress- and mitogen-activated protein (MAP) kinases, p38 and JNK, are at the nexus of numerous stress responses, among these the ribotoxic stress response (RSR). Ribosomal impairment is detrimental to cell function as it disrupts protein synthesis, increase inflammatory signaling and, if unresolved, lead to cell death. In this review, we offer a general overview of the three main translation surveillance pathways; the RSR, Ribosome-associated Quality Control (RQC) and the Integrated Stress Response (ISR). We highlight recent advances made in defining activation mechanisms for these pathways and discuss their commonalities and differences. Finally, we reflect on the physiological role of the RSR and consider the therapeutic potential of targeting the sensing kinase ZAKα for treatment of ribotoxin exposure.

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Herpesviruses and the Unfolded Protein Response

10.20944/preprints201912.0040.v1 ◽

2019 ◽

Cited By ~ 1

Author(s):

Benjamin P. Johnston ◽

Craig McCormick

Keyword(s):

Stress Response ◽

Viral Replication ◽

Unfolded Protein Response ◽

Stress Responses ◽

Cellular Stress ◽

Cellular Stress Response ◽

Negative Effects ◽

Unfolded Protein ◽

The Unfolded Protein Response ◽

Protein Response

Herpesviruses usurp cellular stress responses to avoid immune detection while simultaneously promoting viral replication and spread. The unfolded protein response (UPR) is an evolutionarily conserved stress response that is activated when the protein load in the ER saturates its chaperone folding capacity causing an accrual of misfolded proteins. Through translational and transcriptional reprogramming, the UPR aims to restore protein homeostasis; however, if this fails the cell undergoes apoptosis. It is commonly thought that many enveloped viruses, including herpesviruses, may activate the UPR due to saturation of the ER with nascent glycoproteins and thus these viruses may have evolved mechanisms to evade the potentially negative effects of UPR signaling. Over the past fifteen years there has been considerable effort to provide evidence that different viruses may reprogram the UPR to promote viral replication. Here we provide an overview of the molecular events of UPR activation, signaling and transcriptional outputs, and highlight key findings that demonstrate that the UPR is an important cellular stress response that herpesviruses have hijacked to facilitate persistent infection.

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Functional correlates of negative effects of allostatic load with long-term adaptation to labor factors

Russian Journal of Occupational Health and Industrial Ecology ◽

10.31089/1026-9428-2019-59-9-682-683 ◽

2020 ◽

pp. 682-682

Author(s):

T. D. Lipenetskaia

Keyword(s):

Allostatic Load ◽

External Exposure ◽

Negative Effects

Under certain conditions of strong or prolonged external exposure, signs of either allostatic load or allostatic load are formed. The question of the different physiological nature of these states is discussed.

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Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders

Biomedicines ◽

10.3390/biomedicines9020099 ◽

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

Microorganisms ◽

10.3390/microorganisms9061116 ◽

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.

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A microbiota–root–shoot circuit favours Arabidopsis growth over defence under suboptimal light

Nature Plants ◽

10.1038/s41477-021-00956-4 ◽

2021 ◽

Author(s):

Shiji Hou ◽

Thorsten Thiergart ◽

Nathan Vannier ◽

Fantin Mesny ◽

Jörg Ziegler ◽

...

Keyword(s):

Stress Responses ◽

Photosynthetically Active Radiation ◽

Bacterial Community Composition ◽

Light Condition ◽

Long Distance ◽

Active Radiation ◽

Light Manipulation ◽

Growth Deficiency ◽

Dependent Growth ◽

Control Light

AbstractBidirectional root–shoot signalling is probably key in orchestrating stress responses and ensuring plant survival. Here, we show that Arabidopsis thaliana responses to microbial root commensals and light are interconnected along a microbiota–root–shoot axis. Microbiota and light manipulation experiments in a gnotobiotic plant system reveal that low photosynthetically active radiation perceived by leaves induces long-distance modulation of root bacterial communities but not fungal or oomycete communities. Reciprocally, microbial commensals alleviate plant growth deficiency under low photosynthetically active radiation. This growth rescue was associated with reduced microbiota-induced aboveground defence responses and altered resistance to foliar pathogens compared with the control light condition. Inspection of a set of A. thaliana mutants reveals that this microbiota- and light-dependent growth–defence trade-off is directly explained by belowground bacterial community composition and requires the host transcriptional regulator MYC2. Our work indicates that aboveground stress responses in plants can be modulated by signals from microbial root commensals.

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Clade III cytokinin response factors share common roles in response to oxidative stress responses linked to cytokinin synthesis

Journal of Experimental Botany ◽

10.1093/jxb/erab076 ◽

2021 ◽

Vol 72 (8) ◽

pp. 3294-3306

Author(s):

Ariel M Hughes ◽

H Tucker Hallmark ◽

Lenka Plačková ◽

Ondrej Novák ◽

Aaron M Rashotte

Keyword(s):

Oxidative Stress ◽

Transcription Factors ◽

Stress Response ◽

Stress Responses ◽

Oxidative Stress Response ◽

Response Factors ◽

Ontology Term ◽

Regulated Expression ◽

Cytokinin Response ◽

Oxidative Stress Responses

Abstract Cytokinin response factors (CRFs) are transcription factors that are involved in cytokinin (CK) response, as well as being linked to abiotic stress tolerance. In particular, oxidative stress responses are activated by Clade III CRF members, such as AtCRF6. Here we explored the relationships between Clade III CRFs and oxidative stress. Transcriptomic responses to oxidative stress were determined in two Clade III transcription factors, Arabidopsis AtCRF5 and tomato SlCRF5. AtCRF5 was required for regulated expression of >240 genes that are involved in oxidative stress response. Similarly, SlCRF5 was involved in the regulated expression of nearly 420 oxidative stress response genes. Similarities in gene regulation by these Clade III members in response to oxidative stress were observed between Arabidopsis and tomato, as indicated by Gene Ontology term enrichment. CK levels were also changed in response to oxidative stress in both species. These changes were regulated by Clade III CRFs. Taken together, these findings suggest that Clade III CRFs play a role in oxidative stress response as well as having roles in CK signaling.

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Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules

Biomolecules ◽

10.3390/biom11020266 ◽

2021 ◽

Vol 11 (2) ◽

pp. 266

Author(s):

Chiara Lanzillotta ◽

Fabio Di Domenico

Keyword(s):

Down Syndrome ◽

Stress Response ◽

Stress Responses ◽

Redox Balance ◽

Antioxidant Response ◽

Chromosome 21 ◽

Therapeutic Approaches ◽

Genomic Disorder ◽

Therapeutic Molecules ◽

Early Alzheimer’S Disease

Down syndrome (DS) is the most common genomic disorder characterized by the increased incidence of developing early Alzheimer’s disease (AD). In DS, the triplication of genes on chromosome 21 is intimately associated with the increase of AD pathological hallmarks and with the development of brain redox imbalance and aberrant proteostasis. Increasing evidence has recently shown that oxidative stress (OS), associated with mitochondrial dysfunction and with the failure of antioxidant responses (e.g., SOD1 and Nrf2), is an early signature of DS, promoting protein oxidation and the formation of toxic protein aggregates. In turn, systems involved in the surveillance of protein synthesis/folding/degradation mechanisms, such as the integrated stress response (ISR), the unfolded stress response (UPR), and autophagy, are impaired in DS, thus exacerbating brain damage. A number of pre-clinical and clinical studies have been applied to the context of DS with the aim of rescuing redox balance and proteostasis by boosting the antioxidant response and/or inducing the mechanisms of protein re-folding and clearance, and at final of reducing cognitive decline. So far, such therapeutic approaches demonstrated their efficacy in reverting several aspects of DS phenotype in murine models, however, additional studies aimed to translate these approaches in clinical practice are still needed.

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