AtHsfA2 modulates expression of stress responsive genes and enhances tolerance to heat and oxidative stress in Arabidopsis

Li, Chunguang; Chen, Qijun; Gao, Xin-Qi; Qi, Bishu; Chen, Naizhi; Xu, Shengjie; Chen, Jia; Wang, Xuechen

doi:10.1360/062005-119

Cited by 91 publications

(86 citation statements)

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“…HsfA2 plays an important role in acquired thermotolerance and also appears to play a role in abiotic stress tolerance. Indeed, some studies have reported the role of HsfA2 in oxidative stress (Li et al, 2005), high light conditions and chilling (Nishizawa et al, 2006(Nishizawa et al, , 2008, and salt/osmotic stress tolerance, suggesting a role in multiple stress tolerance (Ogawa et al, 2007). The results obtained through a genetic approach demonstrate that the hsfA2 mutant cannot cross-acclimate to anoxia through mild heat pretreatment, in contrast to the wild type (Fig.…”

Section: Discussionmentioning

confidence: 91%

“…Interestingly, it seems that in Arabidopsis, different from tomato (Solanum lycopersicum; Mishra et al, 2002), there is not a unique master regulator for the Hsf-mediated heat shock response. Different Hsfs have been identified as potential crucial element for Arabidopsis response not only to heat stress (Busch et al, 2005;Schramm et al, 2006Schramm et al, , 2008Charng et al, 2007) but also to oxidative stress (Li et al, 2005;Nishizawa et al, 2008), hydrogen peroxide (H 2 O 2 ), high light (Nishizawa et al, 2006), and salt stress as well (Ogawa et al, 2007).…”

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confidence: 99%

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The Heat-Inducible Transcription Factor HsfA2 Enhances Anoxia Tolerance in Arabidopsis

et al. 2010

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Anoxia induces several heat shock proteins, and a mild heat pretreatment can acclimatize Arabidopsis (Arabidopsis thaliana) seedlings to subsequent anoxic treatment. In this study, we analyzed the response of Arabidopsis seedlings to anoxia, heat, and combined heat + anoxia stress. A significant overlap between the anoxic and the heat responses was observed by wholegenome microarray analysis. Among the transcription factors induced by both heat and anoxia, the heat shock factor A2 (HsfA2), known to be involved in Arabidopsis acclimation to heat and to other abiotic stresses, was strongly induced by anoxia. Heat-dependent acclimation to anoxia is lost in an HsfA2 knockout mutant (hsfa2) as well as in a double mutant for the constitutively expressed HsfA1a/HsfA1b (hsfA1a/1b), indicating that these three heat shock factors cooperate to confer anoxia tolerance. Arabidopsis seedlings that overexpress HsfA2 showed an increased expression of several known targets of this transcription factor and were markedly more tolerant to anoxia as well as to submergence. Anoxia failed to induce HsfA2 target proteins in wild-type seedlings, while overexpression of HsfA2 resulted in the production of HsfA2 targets under anoxia, correlating well with the low anoxia tolerance experiments. These results indicate that there is a considerable overlap between the molecular mechanisms of heat and anoxia tolerance and that HsfA2 is a player in these mechanisms.

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Section: Discussionmentioning

confidence: 91%

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confidence: 99%

The Heat-Inducible Transcription Factor HsfA2 Enhances Anoxia Tolerance in Arabidopsis

et al. 2010

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“…These data suggest that HSFA4A is involved in the modulation of ROS metabolism and responses to oxidative stress. HSF-dependent regulation of Apx genes has been previously documented (Panchuk et al, 2002;Li et al, 2005;Banti et al, 2010), underlining the importance of HSFs as mediators of oxidative stress responses.…”

Section: Hsfa4a Confers Salt Tolerance In the Cos Selection Systemmentioning

confidence: 92%

The Heat Shock Factor A4A Confers Salt Tolerance and Is Regulated by Oxidative Stress and the Mitogen-Activated Protein Kinases MPK3 and MPK6

et al. 2014

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Heat shock factors (HSFs) are principal regulators of plant responses to several abiotic stresses. Here, we show that estradioldependent induction of HSFA4A confers enhanced tolerance to salt and oxidative agents, whereas inactivation of HSFA4A results in hypersensitivity to salt stress in Arabidopsis (Arabidopsis thaliana). Estradiol induction of HSFA4A in transgenic plants decreases, while the knockout hsfa4a mutation elevates hydrogen peroxide accumulation and lipid peroxidation. Overexpression of HSFA4A alters the transcription of a large set of genes regulated by oxidative stress. In yeast (Saccharomyces cerevisiae) two-hybrid and bimolecular fluorescence complementation assays, HSFA4A shows homomeric interaction, which is reduced by alanine replacement of three conserved cysteine residues. HSFA4A interacts with mitogen-activated protein kinases MPK3 and MPK6 in yeast and plant cells. MPK3 and MPK6 phosphorylate HSFA4A in vitro on three distinct sites, serine-309 being the major phosphorylation site. Activation of the MPK3 and MPK6 mitogen-activated protein kinase pathway led to the transcriptional activation of the HEAT SHOCK PROTEIN17.6A gene. In agreement that mutation of serine-309 to alanine strongly diminished phosphorylation of HSFA4A, it also strongly reduced the transcriptional activation of HEAT SHOCK PROTEIN17.6A. These data suggest that HSFA4A is a substrate of the MPK3/MPK6 signaling and that it regulates stress responses in Arabidopsis.

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“…The disruption of HsfA2 caused a slight reduction in expression of some Hsp genes upon HS treatment and that the knockout mutant displayed reduced basal and AT as well as oxidative stress tolerance, while overexpression of HsfA2 enhances tolerance under these stress conditions [85]. Schramm et al [86] identified a subset of genes whose expression was reduced upon HS treatment in the knockout mutant.…”

Section: Heat-inducible Transcription Factormentioning

confidence: 99%

Heat Stress Responses and Thermotolerance

Hemantaranjan¹,

Bhanu²,

Singh³

et al. 2014

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climate change is that most agricultural regions will experience additional extreme environmental fluctuations [2]. Direct injuries due to high temperatures include protein denaturation and aggregation and increased fluidity of membrane lipids. Indirect or slower heat injuries include inactivation of enzymes in chloroplast and mitochondria, inhibition of protein synthesis, protein degradation and loss of membrane integrity [3]. Heat stress also affects the organization of microtubules by splitting and/or elongation of spindles, formation of microtubule asters in mitotic cells and elongation of phragmoplast microtubules [4].The unfavourable effects of heat stress can be mitigated by developing crop plants with improved thermotolerance using an assortment of genetic approaches. For this reason, a thorough understanding of physiological responses of plants to high temperature, mechanisms of heat tolerance and possible strategies for improving crop thermotolerance is crucial. Acquiring thermotolerance is a lively progression by which considerable amounts of plant resources are diverted to structural and functional maintenance to escape damages caused by heat stress. Although biochemical and molecular aspects of thermotolerance in plants are relatively well understood, additional studies focused on phenotypic flexibility and assimilate partitioning under heat stress and factors modulating crop heat tolerance are imperative. High temperature during seed germination may slow down or totally inhibit germination, depending on plant species and the intensity of the stress [5]. At later stages, high IntroductionFuture global climate change, with predicted 1.5-5.8 °C increases in temperatures by 2100 has to cause heat stress to create threats to agricultural production [1]. An increase in global temperature ranging from 1.1 to 6.4 °C depending on global emissions scenarios, will accompany the rises in atmospheric CO 2 . Though high temperature and other abiotic stresses are clearly limiting factors for crops cultivated on marginal lands, crop productivity far and wide is often at the mercy of random environmental fluctuations. Existing assumption about global Heat Stress Responses and Thermotolerance AbstractThe rising ambient temperature by plant cells is crucial for the timely activation of various molecular defences before the appearance of heat damage. The heat-threshold level varies considerably at different developmental stages. With a view to survive under heat stress, mechanisms of regulation at the molecular level enable plants to prosper. Traditional breeding contributed for improving heat tolerance meagrely. The genetic transformation approach needs to be accelerated that can mitigate harmful effects by developing improved thermotolerance of crop plants. In this background, a thorough understanding of physiological responses of plants to high temperature, mechanisms of heat tolerance and possible strategies is vital. Temperature changes are sensed through cellular responses due to signal transduction into the c...

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AtHsfA2 modulates expression of stress responsive genes and enhances tolerance to heat and oxidative stress in Arabidopsis

Cited by 91 publications

References 44 publications

The Heat-Inducible Transcription Factor HsfA2 Enhances Anoxia Tolerance in Arabidopsis

The Heat-Inducible Transcription Factor HsfA2 Enhances Anoxia Tolerance in Arabidopsis

The Heat Shock Factor A4A Confers Salt Tolerance and Is Regulated by Oxidative Stress and the Mitogen-Activated Protein Kinases MPK3 and MPK6

Heat Stress Responses and Thermotolerance

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