Redox control of AP-1-like factors in yeast and beyond

Toone, W. Mark; Morgan, Brian A.; Jones, Nic

doi:10.1038/sj.onc.1204384

Cited by 156 publications

(136 citation statements)

References 80 publications

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“…The accumulation of SKN-1 in intestinal nuclei in response to oxidative stress ( Fig. 5G; Table 3) may parallel nuclear accumulation of Nrf proteins, Yap1p, and Pap1p, under these conditions (Itoh et al 1999;Toone et al 2001;Delaunay et al 2002). It is possible that the intestinal abnormalities in skn-1(zu67)/ nDf41 larvae (Bowerman et al 1992) involve oxidative stress, because 10%-20% of gcs-1(RNAi) animals also die as larvae with abnormal intestines (data not shown).…”

Section: A Conserved Postembryonic Function For Skn-1 In Oxidative Stmentioning

confidence: 95%

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SKN-1 linksC. elegansmesendodermal specification to a conserved oxidative stress response

An¹,

Blackwell²

2003

Genes Dev.

661

877

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During the earliest stages of Caenorhabditis elegans embryogenesis, the transcription factor SKN-1 initiates development of the digestive system and other mesendodermal tissues. Postembryonic SKN-1 functions have not been elucidated. SKN-1 binds to DNA through a unique mechanism, but is distantly related to basic leucine-zipper proteins that orchestrate the major oxidative stress response in vertebrates and yeast. Here we show that despite its distinct mode of target gene recognition, SKN-1 functions similarly to resist oxidative stress in C. elegans. During postembryonic stages, SKN-1 regulates a key Phase II detoxification gene through constitutive and stress-inducible mechanisms in the ASI chemosensory neurons and intestine, respectively. SKN-1 is present in ASI nuclei under normal conditions, and accumulates in intestinal nuclei in response to oxidative stress. skn-1 mutants are sensitive to oxidative stress and have shortened lifespans. SKN-1 represents a connection between developmental specification of the digestive system and one of its most basic functions, resistance to oxidative and xenobiotic stress. This oxidative stress response thus appears to be both widely conserved and ancient, suggesting that the mesendodermal specification role of SKN-1 was predated by its function in these detoxification mechanisms.

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Section: A Conserved Postembryonic Function For Skn-1 In Oxidative Stmentioning

confidence: 95%

“…Nrf-related bZIP proteins regulate Phase II genes in Saccharomyces cerevisiae (Yap1p) and Schizosaccharomyces pombe (Pap1p; Toone et al 2001), suggesting that this ROS response may be generally conserved among eukaryotes. It has therefore been perplexing that bZIP orthologs of these proteins are not present in C. elegans.…”

mentioning

confidence: 99%

SKN-1 linksC. elegansmesendodermal specification to a conserved oxidative stress response

An¹,

Blackwell²

2003

Genes Dev.

661

877

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“…Txn1 is also required for DNA-binding activity of the transcription factors NFκB, AP1, steroid hormone receptors, and p53 [1,[28][29][30]. In yeast exposed to oxidants, dithiol-disulfide exchange reactions between Txn, glutathione peroxidase, and the AP-1 family transcription factor YAP1, results in oxidative activation of YAP1 and induction of downstream genes [31].…”

Section: Introductionmentioning

confidence: 99%

Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome

Bondareva¹,

Capecchi²,

Iverson³

et al. 2007

Free Radical Biology and Medicine

102

115

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Thioredoxin reductases (Txnrd)1 maintain intracellular redox homeostasis in most organisms. Metazoans Txnrds also participate in signal transduction. Mouse embryos homozygous for a targeted null mutation of the txnrd1 gene, encoding the cytosolic thioredoxin reductase, were viable at embryonic day 8.5 (E8.5) but not at E9.5. Histology revealed that txnrd1 −/− cells were capable of proliferation and differentiation; however, mutant embryos were smaller than wild-type littermates and failed to gastrulate. In situ marker gene analyses indicated primitive streak mesoderm did not form. Microarray analyses on E7.5 txnrd −/− and txnrd +/+ littermates showed similar mRNA levels for peroxiredoxins, glutathione reductases, mitochondrial Txnrd2, and most markers of cell proliferation. Conversely, mRNAs encoding sulfiredoxin, IGF-binding protein 1, carbonyl reductase 3, glutamate cysteine ligase, glutathione S-transferases, and metallothioneins were more abundant in mutants. Many gene expression responses mirrored those in thioredoxin reductase 1-null yeast; however mice exhibited a novel response within the peroxiredoxin catalytic cycle. Thus, whereas yeast induce peroxiredoxin mRNAs in response to thioredoxin reductase disruption, mice induced sulfiredoxin mRNA. In summary, Txnrd1 was required for correct patterning of the early embryo and progression to later development. Conserved responses to Txnrd1 disruption likely allowed proliferation and limited differentiation of the mutant embryo cells.

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“…It possesses a variety of biological functions including the ability to modulate the DNA binding activity of the ligand-activated transcription factor aryl hydrocarbon receptor (AHR) as well as the activity of several other transcription factors including general transcription factor IIIC, NF-κB, and AP-1 [64,65]. Reactive oxygen species generated through cellular metabolism can function as cellular second messengers through the regulation of numerous signal transduction pathways.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Smith

Shaw

et al. 2004

BMC Immunol

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BackgroundChemokines are involved in many biological activities ranging from leukocyte differentiation to neuronal morphogenesis. Despite numerous reports describing chemokine function, little is known about the molecular changes induced by cytokines.MethodsWe have isolated and identified by differential display analysis 182 differentially expressed cDNAs from CXCR3-transfected Jurkat T cells following treatment with CXCL12 or CXCL10. These chemokine-modulated genes were further verified using quantitative RT-PCR and Western blot analysis.ResultsOne hundred and forty-six of the cDNAs were successfully cloned, sequenced, and identified by BLAST. Following removal of redundant and non-informative clones, seventeen mRNAs were found to be differentially expressed post treatment with either chemokine ligand with several representing known genes with established functions. Twenty-one genes were upregulated in these transfected Jurkat cells following both CXCL12 and CXCL10, four genes displayed a discordant response and seven genes were downregulated upon treatment with either chemokine. Identified genes include geminin (GEM), thioredoxin (TXN), DEAD/H box polypeptide 1 (DDX1), growth hormone inducible transmembrane protein (GHITM), and transcription elongation regulator 1 (TCERG1). Subsequent analysis of several of these genes using semi-quantitative PCR and western blot analysis confirmed their differential expression post ligand treatment.ConclusionsTogether, these results provide insight into chemokine-induced gene activation and identify potentially novel functions for known genes in chemokine biology.

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Redox control of AP-1-like factors in yeast and beyond

Cited by 156 publications

References 80 publications

SKN-1 linksC. elegansmesendodermal specification to a conserved oxidative stress response

SKN-1 linksC. elegansmesendodermal specification to a conserved oxidative stress response

Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome

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