Document Detail


HIF-1 is required for heat acclimation in the nematode Caenorhabditis elegans.
MedLine Citation:
PMID:  12686697     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic exposure to environmental heat improves tolerance via heat acclimation (AC). Our previous data on mammals indicate that reprogramming the expression of genes coding for stress proteins and energy-metabolism enzymes plays a major role. Knowledge of pathways leading to AC is limited. For their identification, we established a Caenorhabditis elegans AC model and tested mutants in which signaling pathways pertinent to acclimatory responses are mutated. AC attained by maintaining adult C. elegans at 25 degrees C for 18 h enhanced heat endurance of wild-type worms subjected to heat stress (35 degrees C) and conferred protection against hypoxia and cadmium. Survival curves demonstrated that both daf-2 (insulin receptor pathway) showing enhanced heat tolerance and daf-16 loss-of-function (a transcription factor mediating DAF-2 signaling) mutants benefit from AC, suggesting that the insulin receptor pathway does not mediate AC. In contrast, the hif-1 (hypoxia inducible factor) loss-of-function strain did not show acclimation, and non-acclimated vhl-1 and egl-9 mutants (overexpressing HIF-1) had greater heat endurance than the wild type. Like mammals, HIF-1 and HSP72 levels increased in the wild-type AC nematodes. HSP72 upregulation in AC hif-1 mutants was also observed; however, it was insufficient to improve heat/stress tolerance, suggesting that HIF-1 upregulation is essential for acclimation, whereas HSP72 upregulation in the absence of HIF-1 is inadequate. We conclude that HIF-1 upregulation is both an evolutionarily conserved and a necessary component of heat acclimation. The known targets of HIF-1 imply that metabolic adaptations are essential for AC-dependent tolerance to heat and heavy metals, in addition to their known role in hypoxic adaptation.
Authors:
Millet Treinin; Judith Shliar; Huaqi Jiang; Jo Anne Powell-Coffman; Zohar Bromberg; Michal Horowitz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2003-06-24
Journal Detail:
Title:  Physiological genomics     Volume:  14     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-25     Completed Date:  2003-08-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  17-24     Citation Subset:  IM    
Affiliation:
Department of Physiology, Hadassah Medical School, Jerusalem 91120, Israel.
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MeSH Terms
Descriptor/Qualifier:
Acclimatization / genetics,  physiology*
Animals
Cadmium / metabolism
Caenorhabditis elegans / genetics,  physiology*
Caenorhabditis elegans Proteins / biosynthesis,  genetics,  physiology*
DNA-Binding Proteins / biosynthesis,  genetics,  physiology*
Gene Expression Regulation / physiology
Genes, Helminth / genetics,  physiology
Hot Temperature*
Hypoxia-Inducible Factor 1
Metals, Heavy / metabolism
Mutation
Nuclear Proteins / biosynthesis,  genetics,  physiology*
Phenotype
Receptor, Insulin / physiology
Signal Transduction / genetics,  physiology
Survival Analysis
Transcription Factors*
Chemical
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/DAF-2 protein, C elegans; 0/DNA-Binding Proteins; 0/Hypoxia-Inducible Factor 1; 0/Metals, Heavy; 0/Nuclear Proteins; 0/Transcription Factors; 7440-43-9/Cadmium; EC 2.7.10.1/Receptor, Insulin
Comments/Corrections
Comment In:
Physiol Genomics. 2003 Jun 24;14(1):1-2   [PMID:  12824472 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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