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Fuyuki Ishikawa - One of the best experts on this subject based on the ideXlab platform.
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hira a conserved histone chaperone plays an essential role in low dose stress response via transcriptional stimulation in fission yeast
Journal of Biological Chemistry, 2012Co-Authors: Moeko Chujo, Yusuke Tarumoto, Koichi Miyatake, Eisuke Nishida, Fuyuki IshikawaAbstract:Cells that have been pre-exposed to mild stress (priming stress) acquire transient resistance to subsequent severe stress even under different combinations of stresses. This phenomenon is called Cross-Tolerance. Although it has been reported that Cross-Tolerance occurs in many organisms, the molecular basis is not clear yet. Here, we identified slm9+ as a responsible gene for the Cross-Tolerance in the fission yeast Schizosaccharomyces pombe. Slm9 is a homolog of mammalian HIRA histone chaperone. HIRA forms a conserved complex and gene disruption of other HIRA complex components, Hip1, Hip3, and Hip4, also yielded a Cross-Tolerance-defective phenotype, indicating that the fission yeast HIRA is involved in the Cross-Tolerance as a complex. We also revealed that Slm9 was recruited to the stress-responsive gene loci upon stress treatment in an Atf1-dependent manner. The expression of stress-responsive genes under stress conditions was compromised in HIRA disruptants. Consistent with this, Pol II recruitment and nucleosome eviction at these gene loci were impaired in slm9Δ cells. Furthermore, we found that the priming stress enhanced the expression of stress-responsive genes in wild-type cells that were exposed to the severe stress. These observations suggest that HIRA functions in stress response through transcriptional regulation. Background: HIRA is a conserved histone chaperone required for regulation of chromatin structure. Results: Genes that encode HIRA proteins are responsible for Cross-Tolerance. Specifically, stress-responsive gene expression was most profoundly compromised in HIRA disruptants. Conclusion: HIRA is involved in Cross-Tolerance via regulation of stress-responsive gene expression. Significance: This study provides evidence that fission yeast HIRA functions in stress response.
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HIRA, a Conserved Histone Chaperone, Plays an Essential Role in Low-dose Stress Response via Transcriptional Stimulation in Fission Yeast
Journal of Biological Chemistry, 2012Co-Authors: Moeko Chujo, Yusuke Tarumoto, Koichi Miyatake, Eisuke Nishida, Fuyuki IshikawaAbstract:Cells that have been pre-exposed to mild stress (priming stress) acquire transient resistance to subsequent severe stress even under different combinations of stresses. This phenomenon is called Cross-Tolerance. Although it has been reported that Cross-Tolerance occurs in many organisms, the molecular basis is not clear yet. Here, we identified slm9+ as a responsible gene for the Cross-Tolerance in the fission yeast Schizosaccharomyces pombe. Slm9 is a homolog of mammalian HIRA histone chaperone. HIRA forms a conserved complex and gene disruption of other HIRA complex components, Hip1, Hip3, and Hip4, also yielded a Cross-Tolerance-defective phenotype, indicating that the fission yeast HIRA is involved in the Cross-Tolerance as a complex. We also revealed that Slm9 was recruited to the stress-responsive gene loci upon stress treatment in an Atf1-dependent manner. The expression of stress-responsive genes under stress conditions was compromised in HIRA disruptants. Consistent with this, Pol II recruitment and nucleosome eviction at these gene loci were impaired in slm9Δ cells. Furthermore, we found that the priming stress enhanced the expression of stress-responsive genes in wild-type cells that were exposed to the severe stress. These observations suggest that HIRA functions in stress response through transcriptional regulation.
Christine H Foyer - One of the best experts on this subject based on the ideXlab platform.
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Cross Tolerance to biotic and abiotic stresses in plants a focus on resistance to aphid infestation
Journal of Experimental Botany, 2016Co-Authors: Christine H Foyer, Brwa Rasool, Jack W Davey, Robert D HancockAbstract:Plants co-evolved with an enormous variety of microbial pathogens and insect herbivores under daily and seasonal variations in abiotic environmental conditions. Hence, plant cells display a high capacity to respond to diverse stresses through a flexible and finely balanced response network that involves components such as reduction-oxidation (redox) signalling pathways, stress hormones and growth regulators, as well as calcium and protein kinase cascades. Biotic and abiotic stress responses use common signals, pathways and triggers leading to Cross-Tolerance phenomena, whereby exposure to one type of stress can activate plant responses that facilitate Tolerance to several different types of stress. While the acclimation mechanisms and adaptive responses that facilitate responses to single biotic and abiotic stresses have been extensively characterized, relatively little information is available on the dynamic aspects of combined biotic/abiotic stress response. In this review, we consider how the abiotic environment influences plant responses to attack by phloem-feeding aphids. Unravelling the signalling cascades that underpin Cross-Tolerance to biotic and abiotic stresses will allow the identification of new targets for increasing environmental resilience in crops.
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the impact of global change factors on redox signaling underpinning stress Tolerance
Plant Physiology, 2013Co-Authors: Sergi Munnebosch, Guillaume Queval, Christine H FoyerAbstract:Reduction/oxidation (redox) metabolism and associated signaling are key components of Cross Tolerance to biotic and abiotic stresses in plants. Climate change factors such as predicted increases in temperature and the availability of atmospheric carbon dioxide ([CO2][1]) and ozone ([O3][2]) will
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common components networks and pathways of Cross Tolerance to stress the central role of redox and abscisic acid mediated controls
Plant Physiology, 2002Co-Authors: G M Pastori, Christine H FoyerAbstract:The vigor and responsiveness of plants to environmental stress result from the constant re-adjustment of physiology and metabolism throughout the life cycle within the framework of the genetic background. Plants have developed unique strategies for responding to ever-changing environmental conditions, exhaustively monitoring their surroundings and adjusting their metabolic systems to maintain homeostasis. The severity of stress, the genetic background of the plant, and its individual history determine everyday survival or death. These factors dictate the destiny of any individual. The genomeenvironment interaction is, therefore, an essential focus for the elucidation of the nature of the phenotypic variation leading to the successful response of plants to environmental cues. Plants acclimate to biotic and abiotic stresses by triggering a cascade or network of events that starts with stress perception and ends with the expression of a battery of target genes. The key components of the stress-response relationship are illustrated in Fig. 1. These are stress stimulus, signals, transducers, transcription regulators, target genes, and stress responses, including morphological, biochemical, and physiological changes. In evolutionary terms, components that are near to the end of the stressresponse cascade are not predicted to be the ones whose actions significantly affect the operation of other genes. However, factors that act at early stages are critical for other cell functions. Plants make use of common pathways and components in the stressresponse relationship. This phenomenon, which is known as Cross-Tolerance, allows plants to adapt/ acclimate to a range of different stresses after exposure to one specific stress. The major focus of this review, therefore, concerns the basic features of signaling that underpin Cross-Tolerance and result from the action of common elements, which are likely to occur early in the stress response cascade. First, using drought and chilling as examples, we explore the evidence for common signals and elements that confer Cross-Tolerance. Second, we highlight the importance of “redox signals” in such networks and discuss the evidence to date for the existence of such pathways in plants. The elucidation of common components has enormous potential and has, therefore, become a priority in research and breeding programs aimed at improving plant stress Tolerance.
Moeko Chujo - One of the best experts on this subject based on the ideXlab platform.
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hira a conserved histone chaperone plays an essential role in low dose stress response via transcriptional stimulation in fission yeast
Journal of Biological Chemistry, 2012Co-Authors: Moeko Chujo, Yusuke Tarumoto, Koichi Miyatake, Eisuke Nishida, Fuyuki IshikawaAbstract:Cells that have been pre-exposed to mild stress (priming stress) acquire transient resistance to subsequent severe stress even under different combinations of stresses. This phenomenon is called Cross-Tolerance. Although it has been reported that Cross-Tolerance occurs in many organisms, the molecular basis is not clear yet. Here, we identified slm9+ as a responsible gene for the Cross-Tolerance in the fission yeast Schizosaccharomyces pombe. Slm9 is a homolog of mammalian HIRA histone chaperone. HIRA forms a conserved complex and gene disruption of other HIRA complex components, Hip1, Hip3, and Hip4, also yielded a Cross-Tolerance-defective phenotype, indicating that the fission yeast HIRA is involved in the Cross-Tolerance as a complex. We also revealed that Slm9 was recruited to the stress-responsive gene loci upon stress treatment in an Atf1-dependent manner. The expression of stress-responsive genes under stress conditions was compromised in HIRA disruptants. Consistent with this, Pol II recruitment and nucleosome eviction at these gene loci were impaired in slm9Δ cells. Furthermore, we found that the priming stress enhanced the expression of stress-responsive genes in wild-type cells that were exposed to the severe stress. These observations suggest that HIRA functions in stress response through transcriptional regulation. Background: HIRA is a conserved histone chaperone required for regulation of chromatin structure. Results: Genes that encode HIRA proteins are responsible for Cross-Tolerance. Specifically, stress-responsive gene expression was most profoundly compromised in HIRA disruptants. Conclusion: HIRA is involved in Cross-Tolerance via regulation of stress-responsive gene expression. Significance: This study provides evidence that fission yeast HIRA functions in stress response.
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HIRA, a Conserved Histone Chaperone, Plays an Essential Role in Low-dose Stress Response via Transcriptional Stimulation in Fission Yeast
Journal of Biological Chemistry, 2012Co-Authors: Moeko Chujo, Yusuke Tarumoto, Koichi Miyatake, Eisuke Nishida, Fuyuki IshikawaAbstract:Cells that have been pre-exposed to mild stress (priming stress) acquire transient resistance to subsequent severe stress even under different combinations of stresses. This phenomenon is called Cross-Tolerance. Although it has been reported that Cross-Tolerance occurs in many organisms, the molecular basis is not clear yet. Here, we identified slm9+ as a responsible gene for the Cross-Tolerance in the fission yeast Schizosaccharomyces pombe. Slm9 is a homolog of mammalian HIRA histone chaperone. HIRA forms a conserved complex and gene disruption of other HIRA complex components, Hip1, Hip3, and Hip4, also yielded a Cross-Tolerance-defective phenotype, indicating that the fission yeast HIRA is involved in the Cross-Tolerance as a complex. We also revealed that Slm9 was recruited to the stress-responsive gene loci upon stress treatment in an Atf1-dependent manner. The expression of stress-responsive genes under stress conditions was compromised in HIRA disruptants. Consistent with this, Pol II recruitment and nucleosome eviction at these gene loci were impaired in slm9Δ cells. Furthermore, we found that the priming stress enhanced the expression of stress-responsive genes in wild-type cells that were exposed to the severe stress. These observations suggest that HIRA functions in stress response through transcriptional regulation.
Charles E Mccall - One of the best experts on this subject based on the ideXlab platform.
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lipopolysaccharide and lipoteichoic acid induced Tolerance and Cross Tolerance distinct alterations in il 1 receptor associated kinase
Journal of Immunology, 2002Co-Authors: Randy Jacinto, Thomas Hartung, Charles E MccallAbstract:Human Toll-like receptor (TLR) 4 and TLR2 receptors recognize LPS or lipoteichoic acid (LTA), respectively. Prolonged exposure of human macrophages/monocytes to bacterial LPS induces a state of adaptation/Tolerance to subsequent LPS challenge. Inflammatory gene expressions such as IL-1beta and TNF-alpha are selectively repressed, while certain anti-inflammatory genes such as secretory IL-1R antagonist are still induced in LPS-adapted/tolerant cells. In this report, we demonstrate that LPS-tolerized human promonocytic THP-1 cells develop Cross-Tolerance and no longer respond to LTA-induced IL-1beta/TNF-alpha production, indicating that disruption of common intracellular signaling is responsible for the decreased IL-1beta/TNF-alpha production. We observe that down-regulation of IL-1R-associated kinase (IRAK) protein level and kinase activity closely correlates with the development of Cross-Tolerance. IRAK protein levels and kinase activities in LPS-tolerized cells remain low and hyporesponsive to subsequent LPS or LTA challenges. We also demonstrate that THP-1 cells with prolonged LTA treatment develop LTA Tolerance and do not express IL-1beta/TNF-alpha upon further LTA challenge. Strikingly, cells tolerized with LTA are only refractory to subsequent LTA challenge and can still respond to LPS stimulation. Correspondingly, stimulation of TLR2 by LTA, although activating IRAK, does not cause IRAK degradation. IRAK from LTA-tolerized cells can be subsequently activated and degraded by further LPS challenge, but not LTA treatment. Our studies reveal that LTA-induced Tolerance is distinct compared with that of LPS Tolerance, and is likely due to disruption of unique TLR2 signaling components upstream of MyD88/IRAK.
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lipopolysaccharide and lipoteichoic acid induced Tolerance and Cross Tolerance distinct alterations in il 1 receptor associated kinase
Journal of Immunology, 2002Co-Authors: Randy Jacinto, Thomas Hartung, Charles E MccallAbstract:Human Toll-like receptor (TLR) 4 and TLR2 receptors recognize LPS or lipoteichoic acid (LTA), respectively. Prolonged exposure of human macrophages/monocytes to bacterial LPS induces a state of adaptation/Tolerance to subsequent LPS challenge. Inflammatory gene expressions such as IL-1β and TNF-α are selectively repressed, while certain anti-inflammatory genes such as secretory IL-1R antagonist are still induced in LPS-adapted/tolerant cells. In this report, we demonstrate that LPS-tolerized human promonocytic THP-1 cells develop Cross-Tolerance and no longer respond to LTA-induced IL-1β/TNF-α production, indicating that disruption of common intracellular signaling is responsible for the decreased IL-1β/TNF-α production. We observe that down-regulation of IL-1R-associated kinase (IRAK) protein level and kinase activity closely correlates with the development of Cross-Tolerance. IRAK protein levels and kinase activities in LPS-tolerized cells remain low and hyporesponsive to subsequent LPS or LTA challenges. We also demonstrate that THP-1 cells with prolonged LTA treatment develop LTA Tolerance and do not express IL-1β/TNF-α upon further LTA challenge. Strikingly, cells tolerized with LTA are only refractory to subsequent LTA challenge and can still respond to LPS stimulation. Correspondingly, stimulation of TLR2 by LTA, although activating IRAK, does not cause IRAK degradation. IRAK from LTA-tolerized cells can be subsequently activated and degraded by further LPS challenge, but not LTA treatment. Our studies reveal that LTA-induced Tolerance is distinct compared with that of LPS Tolerance, and is likely due to disruption of unique TLR2 signaling components upstream of MyD88/IRAK.
Thomas Hartung - One of the best experts on this subject based on the ideXlab platform.
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lipopolysaccharide and lipoteichoic acid induced Tolerance and Cross Tolerance distinct alterations in il 1 receptor associated kinase
Journal of Immunology, 2002Co-Authors: Randy Jacinto, Thomas Hartung, Charles E MccallAbstract:Human Toll-like receptor (TLR) 4 and TLR2 receptors recognize LPS or lipoteichoic acid (LTA), respectively. Prolonged exposure of human macrophages/monocytes to bacterial LPS induces a state of adaptation/Tolerance to subsequent LPS challenge. Inflammatory gene expressions such as IL-1β and TNF-α are selectively repressed, while certain anti-inflammatory genes such as secretory IL-1R antagonist are still induced in LPS-adapted/tolerant cells. In this report, we demonstrate that LPS-tolerized human promonocytic THP-1 cells develop Cross-Tolerance and no longer respond to LTA-induced IL-1β/TNF-α production, indicating that disruption of common intracellular signaling is responsible for the decreased IL-1β/TNF-α production. We observe that down-regulation of IL-1R-associated kinase (IRAK) protein level and kinase activity closely correlates with the development of Cross-Tolerance. IRAK protein levels and kinase activities in LPS-tolerized cells remain low and hyporesponsive to subsequent LPS or LTA challenges. We also demonstrate that THP-1 cells with prolonged LTA treatment develop LTA Tolerance and do not express IL-1β/TNF-α upon further LTA challenge. Strikingly, cells tolerized with LTA are only refractory to subsequent LTA challenge and can still respond to LPS stimulation. Correspondingly, stimulation of TLR2 by LTA, although activating IRAK, does not cause IRAK degradation. IRAK from LTA-tolerized cells can be subsequently activated and degraded by further LPS challenge, but not LTA treatment. Our studies reveal that LTA-induced Tolerance is distinct compared with that of LPS Tolerance, and is likely due to disruption of unique TLR2 signaling components upstream of MyD88/IRAK.
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lipopolysaccharide and lipoteichoic acid induced Tolerance and Cross Tolerance distinct alterations in il 1 receptor associated kinase
Journal of Immunology, 2002Co-Authors: Randy Jacinto, Thomas Hartung, Charles E MccallAbstract:Human Toll-like receptor (TLR) 4 and TLR2 receptors recognize LPS or lipoteichoic acid (LTA), respectively. Prolonged exposure of human macrophages/monocytes to bacterial LPS induces a state of adaptation/Tolerance to subsequent LPS challenge. Inflammatory gene expressions such as IL-1beta and TNF-alpha are selectively repressed, while certain anti-inflammatory genes such as secretory IL-1R antagonist are still induced in LPS-adapted/tolerant cells. In this report, we demonstrate that LPS-tolerized human promonocytic THP-1 cells develop Cross-Tolerance and no longer respond to LTA-induced IL-1beta/TNF-alpha production, indicating that disruption of common intracellular signaling is responsible for the decreased IL-1beta/TNF-alpha production. We observe that down-regulation of IL-1R-associated kinase (IRAK) protein level and kinase activity closely correlates with the development of Cross-Tolerance. IRAK protein levels and kinase activities in LPS-tolerized cells remain low and hyporesponsive to subsequent LPS or LTA challenges. We also demonstrate that THP-1 cells with prolonged LTA treatment develop LTA Tolerance and do not express IL-1beta/TNF-alpha upon further LTA challenge. Strikingly, cells tolerized with LTA are only refractory to subsequent LTA challenge and can still respond to LPS stimulation. Correspondingly, stimulation of TLR2 by LTA, although activating IRAK, does not cause IRAK degradation. IRAK from LTA-tolerized cells can be subsequently activated and degraded by further LPS challenge, but not LTA treatment. Our studies reveal that LTA-induced Tolerance is distinct compared with that of LPS Tolerance, and is likely due to disruption of unique TLR2 signaling components upstream of MyD88/IRAK.
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induction of Cross Tolerance by lipopolysaccharide and highly purified lipoteichoic acid via different toll like receptors independent of paracrine mediators
Journal of Immunology, 2001Co-Authors: Martin D Lehner, Siegfried Morath, Kathrin S Michelsen, Ralf R Schumann, Thomas HartungAbstract:Exposure of macrophages to LPS induces a state of hyporesponsiveness to subsequent stimulation with LPS termed LPS desensitization or Tolerance. To date, it is not known whether similar mechanisms of macrophage refractoriness are induced on contact with components of Gram-positive bacteria. In the present study, we demonstrate that pretreatment with highly purified lipoteichoic acid (LTA) results in suppression of cytokine release on restimulation with LTA in vitro and in vivo in both C3H/HeN and C3H/HeJ mice, but not in macrophages from Toll-like receptor (TLR)-2-deficient mice. Furthermore, desensitization in response to LPS or LTA exposure also inhibits responses to the other stimulus (“Cross-Tolerance”), suggesting that signaling pathways shared by TLR2 and TLR4 are impaired during Tolerance. Finally, we show that LPS- or LTA-induced Cross-Tolerance is not transferred to hyporesponsive cells cocultured with LPS/LTA-responsive macrophages, showing that soluble mediators do not suffice for Tolerance induction in neighboring cells.