scholarly journals Formation and Regulation of Adaptive Response in NematodeCaenorhabditis elegans

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Y.-L. Zhao ◽  
D.-Y. Wang
Keyword(s):  
Adaptive Response ◽  
Food Limitation ◽  
Adaptive Responses ◽  
Response Control ◽  
C Elegans ◽  
Published Evidence ◽  
Low Concentrations ◽  
Cross Adaptation ◽  
Shock Proteins ◽  
Alternative Theories

All organisms respond to environmental stresses (e.g., heavy metal, heat, UV irradiation, hyperoxia, food limitation, etc.) with coordinated adjustments in order to deal with the consequences and/or injuries caused by the severe stress. The nematodeCaenorhabditis elegansoften exerts adaptive responses if preconditioned with low concentrations of agents or stressor. InC. elegans, three types of adaptive responses can be formed: hormesis, cross-adaptation, and dietary restriction. Several factors influence the formation of adaptive responses in nematodes, and some mechanisms can explain their response formation. In particular, antioxidation system, heat-shock proteins, metallothioneins, glutathione, signaling transduction, and metabolic signals may play important roles in regulating the formation of adaptive responses. In this paper, we summarize the published evidence demonstrating that several types of adaptive responses have converged inC. elegansand discussed some possible alternative theories explaining the adaptive response control.

Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver

2006 ◽  
Vol 27 (3) ◽  
pp. 351-361 ◽  
Author(s):  
Siew Hong Lam ◽  
Cecilia Lanny Winata ◽  
Yan Tong ◽  
Svetlana Korzh ◽  
Wen San Lim ◽  
...  
Keyword(s):  
Biological Networks ◽  
Adaptive Response ◽  
Iron Homeostasis ◽  
Specific Information ◽  
Adaptive Responses ◽  
Arsenic Metabolism ◽  
Genes Encoding ◽  
Shock Proteins ◽  
Zebrafish Liver

Arsenic is a prominent environmental toxicant and carcinogen; however, its molecular mechanism of toxicity and carcinogenicity remains poorly understood. In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 15 parts/million (ppm) arsenic [As(V)] for 8–96 h to identify global transcriptional changes and biological networks involved in arsenic-induced adaptive responses in vivo. We found that there was an increase of transcriptional activity associated with metabolism, especially for biosyntheses, membrane transporter activities, cytoplasm, and endoplasmic reticulum in the 96 h of arsenic treatment, while transcriptional programs for proteins in catabolism, energy derivation, and stress response remained active throughout the arsenic treatment. Many differentially expressed genes encoding proteins involved in heat shock proteins, DNA damage/repair, antioxidant activity, hypoxia induction, iron homeostasis, arsenic metabolism, and ubiquitin-dependent protein degradation were identified, suggesting strongly that DNA and protein damage as a result of arsenic metabolism and oxidative stress caused major cellular injury. These findings were comparable with those reported in mammalian systems, suggesting that the zebrafish liver coupled with the available microarray technology present an excellent in vivo toxicogenomic model for investigating arsenic toxicity. We proposed an in vivo, acute arsenic-induced adaptive response model of the zebrafish liver illustrating the relevance of many transcriptional activities that provide both global and specific information of a coordinated adaptive response to arsenic in the liver.

scholarly journals Hormetic Concentrations of Hydrogen Peroxide but Not Ethanol Induce Cross-Adaptation to Different Stresses in Budding Yeast

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Halyna M. Semchyshyn
Keyword(s):  
Hydrogen Peroxide ◽  
Dose Response ◽  
Budding Yeast ◽  
Regulatory Protein ◽  
Colony Growth ◽  
Inhibitory Effect ◽  
Cross Resistance ◽  
Mild Stress ◽  
Low Concentrations ◽  
Cross Adaptation

The biphasic-dose response of microorganisms to hydrogen peroxide is a phenomenon of particular interest in hormesis research. In different animal models, the dose-response curve for ethanol is also nonlinear showing an inhibitory effect at high doses but a stimulatory effect at low doses. In this study, we observed the hormetic-dose response to ethanol in budding yeastS. cerevisiae. Cross-protection is a phenomenon in which exposure to mild stress results in the acquisition of cellular resistance to lethal stress induced by different factors. Since both hydrogen peroxide and ethanol at low concentrations were found to stimulate yeast colony growth, we evaluated the role of one substance in cell cross-adaptation to the other substance as well as some weak organic acid preservatives. This study demonstrates that, unlike ethanol, hydrogen peroxide at hormetic concentrations causes cross-resistance ofS. cerevisiaeto different stresses. The regulatory protein Yap1 plays an important role in the hormetic effects by low concentrations of either hydrogen peroxide or ethanol, and it is involved in the yeast cross-adaptation by low sublethal doses of hydrogen peroxide.

scholarly journals The noncanonical small heat shock protein HSP-17 from Caenorhabditis elegans is a selective protein aggregase

2020 ◽  
Vol 295 (10) ◽  
pp. 3064-3079 ◽  
Author(s):  
Manuel Iburg ◽  
Dmytro Puchkov ◽  
Irving U. Rosas-Brugada ◽  
Linda Bergemann ◽  
Ulrike Rieprecht ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Heat Shock ◽  
Small Heat Shock Protein ◽  
Independent Manner ◽  
C Elegans ◽  
Higher Eukaryotes ◽  
Prolonged Heat ◽  
Shock Proteins ◽  
Excretory Organs

Small heat shock proteins (sHsps) are conserved, ubiquitous members of the proteostasis network. Canonically, they act as “holdases” and buffer unfolded or misfolded proteins against aggregation in an ATP-independent manner. Whereas bacteria and yeast each have only two sHsps in their genomes, this number is higher in metazoan genomes, suggesting a spatiotemporal and functional specialization in higher eukaryotes. Here, using recombinantly expressed and purified proteins, static light-scattering analysis, and disaggregation assays, we report that the noncanonical sHsp HSP-17 of Caenorhabditis elegans facilitates aggregation of model substrates, such as malate dehydrogenase (MDH), and inhibits disaggregation of luciferase in vitro. Experiments with fluorescently tagged HSP-17 under the control of its endogenous promoter revealed that HSP-17 is expressed in the digestive and excretory organs, where its overexpression promotes the aggregation of polyQ proteins and of the endogenous kinase KIN-19. Systemic depletion of hsp-17 shortens C. elegans lifespan and severely reduces fecundity and survival upon prolonged heat stress. HSP-17 is an abundant protein exhibiting opposing chaperone activities on different substrates, indicating that it is a selective protein aggregase with physiological roles in development, digestion, and osmoregulation.

scholarly journals Sensory regulated Wnt production from neurons helps make organ development robust to environmental changes in C. elegans

Development ◽  
2020 ◽  
Vol 147 (14) ◽  
pp. dev186080
Author(s):  
Katarzyna Modzelewska ◽  
Louise Brown ◽  
Joseph Culotti ◽  
Nadeem Moghal
Keyword(s):  
Synaptic Transmission ◽  
Motor Neurons ◽  
Environmental Changes ◽  
Sensory Perception ◽  
Adaptive Responses ◽  
Vulval Development ◽  
Term Survival ◽  
C Elegans ◽  
Signal Production ◽  
Neuronal Functions

ABSTRACTLong-term survival of an animal species depends on development being robust to environmental variations and climate changes. We used C. elegans to study how mechanisms that sense environmental changes trigger adaptive responses that ensure animals develop properly. In water, the nervous system induces an adaptive response that reinforces vulval development through an unknown backup signal for vulval induction. This response involves the heterotrimeric G-protein EGL-30//Gαq acting in motor neurons. It also requires body-wall muscle, which is excited by EGL-30-stimulated synaptic transmission, suggesting a behavioral function of neurons induces backup signal production from muscle. We now report that increased acetylcholine during liquid growth activates an EGL-30-Rho pathway, distinct from the synaptic transmission pathway, that increases Wnt production from motor neurons. We also provide evidence that this neuronal Wnt contributes to EGL-30-stimulated vulval development, with muscle producing a parallel developmental signal. As diverse sensory modalities stimulate motor neurons via acetylcholine, this mechanism enables broad sensory perception to enhance Wnt-dependent development. Thus, sensory perception improves animal fitness by activating distinct neuronal functions that trigger adaptive changes in both behavior and developmental processes.

scholarly journals Knockout of glial channel ACD-1 exacerbates sensory deficits in a C. elegans mutant by regulating calcium levels of sensory neurons

2012 ◽  
Vol 107 (1) ◽  
pp. 148-158 ◽  
Author(s):  
Ying Wang ◽  
Giulia D'Urso ◽  
Laura Bianchi
Keyword(s):  
Sensory Neurons ◽  
Neuronal Excitability ◽  
Sensory Deficits ◽  
C Elegans ◽  
Hypomorphic Allele ◽  
Low Concentrations ◽  
Wide Range ◽  
Gated Channel ◽  
Intracellular Ca

Degenerin/epithelial Na+ channels (DEG/ENaCs) are voltage-independent Na+ or Na+/Ca2+ channels expressed in many tissues and are needed for a wide range of physiological functions, including sensory perception and transepithelial Na+ transport. In the nervous system, DEG/ENaCs are expressed in both neurons and glia. However, the role of glial vs. neuronal DEG/ENaCs remains unclear. We recently reported the characterization of a novel DEG/ENaC in Caenorhabditis elegans that we named ACD-1. ACD-1 is expressed in glial amphid sheath cells. The glial ACD-1, together with the neuronal DEG/ENaC DEG-1, is necessary for acid avoidance and attraction to lysine. We report presently that knockout of acd-1 in glia exacerbates sensory deficits caused by another mutant: the hypomorphic allele of the cGMP-gated channel subunit tax-2. Furthermore, sensory deficits caused by mutations in Gi protein odr-3 and guanylate cyclase daf-11, which regulate the activity of TAX-2/TAX-4 channels, are worsened by knockout of acd-1. We also show that sensory neurons of acd-1 tax-2(p694) double mutants fail to undergo changes in intracellular Ca2+ when animals are exposed to low concentrations of attractant. Finally, we show that exogenous expression of TRPV1 in sensory neurons and exposure to capsaicin rescue sensory deficits of acd-1 tax-2(p694) mutants, suggesting that sensory deficits of these mutants are bypassed by increasing neuronal excitability. Our data suggest a role of glial DEG/ENaC channel ACD-1 in supporting neuronal activity.

scholarly journals DNA Microarray Analyses of the Long-Term Adaptive Response of Escherichia coli to Acetate and Propionate

2003 ◽  
Vol 69 (3) ◽  
pp. 1759-1774 ◽  
Author(s):  
T. Polen ◽  
D. Rittmann ◽  
V. F. Wendisch ◽  
H. Sahm
Keyword(s):  
Escherichia Coli ◽  
Dna Microarray ◽  
Adaptive Response ◽  
Carbon Sources ◽  
Short Chain Fatty Acids ◽  
Adaptive Responses ◽  
General Stress Response ◽  
E Coli ◽  
Short Term Exposure

ABSTRACT In its natural environment, Escherichia coli is exposed to short-chain fatty acids, such as acetic acid or propionic acid, which can be utilized as carbon sources but which inhibit growth at higher concentrations. DNA microarray experiments revealed expression changes during exponential growth on complex medium due to the presence of sodium acetate or sodium propionate at a neutral external pH. The adaptive responses to acetate and propionate were similar and involved genes in three categories. First, the RNA levels for chemotaxis and flagellum genes increased. Accordingly, the expression of chromosomal fliC′-′lacZ and flhDC′-′lacZ fusions and swimming motility increased after adaptation to acetate or propionate. Second, the expression of many genes that are involved in the uptake and utilization of carbon sources decreased, indicating some kind of catabolite repression by acetate and propionate. Third, the expression of some genes of the general stress response increased, but the increases were more pronounced after short-term exposure for this response than for the adaptive response. Adaptation to propionate but not to acetate involved increased expression of threonine and isoleucine biosynthetic genes. The gene expression changes after adaptation to acetate or propionate were not caused solely by uncoupling or osmotic effects but represented specific characteristics of the long-term response of E. coli to either compound.

scholarly journals Revelations from the NematodeCaenorhabditis eleganson the Complex Interplay of Metal Toxicological Mechanisms

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Ebany J. Martinez-Finley ◽  
Michael Aschner
Keyword(s):  
Contemporary Literature ◽  
Model Organism ◽  
Anthropogenic Sources ◽  
C Elegans ◽  
Disease States ◽  
Metal Levels ◽  
Copper Manganese ◽  
Cellular Detoxification ◽  
Detoxification Systems ◽  
Shock Proteins

Metals have been definitively linked to a number of disease states. Due to the widespread existence of metals in our environment from both natural and anthropogenic sources, understanding the mechanisms of their cellular detoxification is of upmost importance. Organisms have evolved cellular detoxification systems including glutathione, metallothioneins, pumps and transporters, and heat shock proteins to regulate intracellular metal levels. The model organism,Caenorhabditis elegans(C. elegans), contains these systems and provides several advantages for deciphering the mechanisms of metal detoxification. This review provides a brief summary of contemporary literature on the various mechanisms involved in the cellular detoxification of metals, specifically, antimony, arsenic, cadmium, copper, manganese, mercury, and depleted uranium using theC. elegansmodel system for investigation and analysis.

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