Differential Hypoxia Response of hsp-16 Genes in the Nematode

Hong, Mingi; Kwon, Jae Young; Shim, Ju Hyun; Lee, Jun-Ho

doi:10.1016/j.jmb.2004.09.077

Cited by 36 publications

(41 citation statements)

References 22 publications

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“…It has recently been shown that hsp16 genes in general (and hsp16-1 in particular) are key targets for regulation by the DAF-16 FOXO transcription factor in the cell ageing pathway, as well as by HSF-1 in the canonical heat-shock pathway [Hsu et al, 2003;Murphy et al, 2003]. Promoter deletion studies reveal binding sites for additional transcription factors responsive to ethanol (or general stress) and to hypoxia -albeit by a HIF-1-independent pathway [Hong et al, 2004]. These reports strongly imply that hsp16-1 occupies a central position in a complex network of interlinked stress-response pathways.…”

Section: Introductionmentioning

confidence: 99%

Continuous wave and simulated GSM exposure at 1.8 W/kg and 1.8 GHz do not induce hsp16‐1 heat‐shock gene expression in Caenorhabditis elegans

Dawe¹,

Nylund²,

Leszczyński³

et al. 2007

Bioelectromagnetics

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Recent data suggest that there might be a subtle thermal explanation for the apparent induction by radiofrequency (RF) radiation of transgene expression from a small heat‐shock protein (hsp16‐1) promoter in the nematode, Caenorhabditis elegans. The RF fields used in the C. elegans study were much weaker (SAR 5–40 mW kg−1) than those routinely tested in many other published studies (SAR ∼2 W kg−1). To resolve this disparity, we have exposed the same transgenic hsp16‐1::lacZ strain of C. elegans (PC72) to higher intensity RF fields (1.8 GHz; SAR ∼1.8 W kg−1). For both continuous wave (CW) and Talk‐pulsed RF exposures (2.5 h at 25 °C), there was no indication that RF exposure could induce reporter expression above sham control levels. Thus, at much higher induced RF field strength (close to the maximum permitted exposure from a mobile telephone handset), this particular nematode heat‐shock gene is not up‐regulated. However, under conditions where background reporter expression was moderately elevated in the sham controls (perhaps as a result of some unknown co‐stressor), we found some evidence that reporter expression may be reduced by ∼15% following exposure to either Talk‐pulsed or CW RF fields. Bioelectromagnetics 29:92–99, 2008. © 2007 Wiley‐Liss, Inc.

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Section: Introductionmentioning

confidence: 99%

Continuous wave and simulated GSM exposure at 1.8 W/kg and 1.8 GHz do not induce hsp16‐1 heat‐shock gene expression in Caenorhabditis elegans

Dawe¹,

Nylund²,

Leszczyński³

et al. 2007

Bioelectromagnetics

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“…binding Protein-Previously, we showed that the sequence CAC(A/T)CT (block I) is required for the HIF-1-independent hypoxia response of hsp-16 genes; we also demonstrated that regulatory proteins bind to block I-containing sequences in vitro (18). To identify the regulatory proteins that bind the hsp-16.1 promoter under hypoxic conditions, we isolated nuclear extracts from worms incubated under hypoxic conditions and applied them to streptavidin affinity columns containing biotin-labeled block I-containing sequences.…”

Section: Identification Of Hmg-12 As a Hypoxia-induced Promoter-mentioning

confidence: 79%

“…In a study on the hypoxia-induced alteration of gene expression in C. elegans hif-1 mutants, it was reported that HIF-1-independent pathways are involved in the adaptation to hypoxia (17). Our previous study also revealed that the response of small heat shock protein hsp-16 genes (hsp-16.1 and hsp- 16.2) to hypoxic conditions is HIF-1-independent and occurs via cis-acting DNA sequences (CAC(A/T)CT), hereafter referred to as "block I," in the promoter region of these genes (18).…”

mentioning

confidence: 96%

Hypoxia-inducible Factor-1 (HIF-1)-independent Hypoxia Response of the Small Heat Shock Protein hsp-16.1 Gene Regulated by Chromatin-remodeling Factors in the Nematode Caenorhabditis elegans

Lee¹,

Lee

2013

Journal of Biological Chemistry

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Background:To characterize an unknown molecular basis of the hif-1-independent hypoxia response, we used the nematode hsp-16.1 gene as a model. Results: HMG-1.2, together with chromatin-remodeling factors and calcium ions, is involved in the hypoxia response of hsp-16.1. Conclusion: Chromatin modification is important for the hypoxia response of hsp-16.1 in an HIF-1-independent manner. Significance: We report an alternative regulatory pathway for the HIF-1-independent hypoxia response.

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“…Although the heatshock factor HSF-1 targets inducible heat-shock genes at elevated temperatures, it also has other functions, as revealed by its wide-ranging RNAi phenotypes [14,15]. These multipathway links are confirmed by the presence of DAF-16 binding sites [14] as well as ethanol-and hypoxia-response elements [16] within the hsp-16.1 promoter, besides the previously identified HSF-1-binding HSEs [17]. These regulatory links show how a single gene can respond to multiple stressors, and how a single stressor can influence multiple outputs (ROS metabolism, metal resistance, chaperone activity and lifespan).…”

Section: The C Elegans Stress-response Networkmentioning

confidence: 97%

“…However, subtler aspects of effector gene regulation by multiple stressors are only now emerging (e.g. for hsp-16.1) [16]. Our aim is to build an understanding of the underlying control logic [24], initially of each SN separately, and ultimately of the whole SRN.…”

Section: Construction Of the Initial Modelmentioning

confidence: 99%

The Stress-Response Network in Animals: Proposals to Develop a Predictive Mathematical Model

Pomerai¹,

Madhamshettiwar²,

Anbalagan³

et al. 2009

TOTOXIJ

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Abstract:Increasing evidence indicates that numerous genetic pathways responding to environmental stress in animals are regulated co-ordinately as well as independently. These stress-response systems should therefore be viewed in holistic terms as a network. As such, their behaviour is susceptible to mathematical modelling using a systems biology approach. This review outlines relevant evidence and describes a newly launched project to develop just such a model using stressresponse data from multiple transgenic strains of C. elegans and D. melanogaster. We hope that our eventual model will be capable of predicting the effects of simple stressor mixtures with reasonable accuracy. To maximise the effectiveness and scope of this model, we appeal for help from colleagues to share reagents and data relevant to this project. We also present preliminary data where RNA interference has implicated the key transcription factor DAF-16 in an unexpected upregulation of cyp-34A9 reporter expression by high cadmium. STRESS RESPONSES AND MIXTURE TOXICITYIn multicellular organisms, the defensive cellular responses evoked by environmental stresses do not result from simple linear pathways, but rather from a network of interlinked pathways with multiple outputs. This makes it difficult to predict the biological effects of multiple stressors acting together, even though this is the normal situation for industrial pollution of soil or water, where several different contaminants are usually present together. There are few studies and no useful predictive models describing the molecular responses of multicellular organisms to several toxicants acting in concert. This is essentially a systems biology problem, requiring integration of complex molecular and toxicological information. Under the auspices of a Major Award from the UK-India Education and Research Initiative (UK-IERI), we intend to develop an in silico model describing the principal elements of a consensus stress response network (SRN) and its in vivo responses to single stressors, using data from two invertebrate model systems, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. This model will be used to predict the likely SRN responses to stressor mixtures, and such predictions will then be tested experimentally in both species so that the model can be refined accordingly. Since the SRN core pathways are highly conserved among animal taxa, general features of this model should find wider application in ecotoxi-*Address correspondence to this author at the School of Biology, Nottingham University, Nottingham NG7 2RD, UK; Tel: (0044) 115 951 3250; Fax: (0044) 115 951 3251; E-mail: david.depomerai@nottingham.ac.uk cology. The dynamic aspects of this model, and in particular its ability to integrate multiple toxicant inputs for predicting likely SRN outputs, distinguish this from a simple map of the regulatory gene-circuits comprising the SRN. THE C. ELEGANS STRESS-RESPONSE NETWORKThe free-living soil nematode, C. elegans, is particularly suitable fo...

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Differential Hypoxia Response of hsp-16 Genes in the Nematode

Cited by 36 publications

References 22 publications

Continuous wave and simulated GSM exposure at 1.8 W/kg and 1.8 GHz do not induce hsp16‐1 heat‐shock gene expression in Caenorhabditis elegans

Continuous wave and simulated GSM exposure at 1.8 W/kg and 1.8 GHz do not induce hsp16‐1 heat‐shock gene expression in Caenorhabditis elegans

Hypoxia-inducible Factor-1 (HIF-1)-independent Hypoxia Response of the Small Heat Shock Protein hsp-16.1 Gene Regulated by Chromatin-remodeling Factors in the Nematode Caenorhabditis elegans

The Stress-Response Network in Animals: Proposals to Develop a Predictive Mathematical Model

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