Plant Responses to High Temperature

Larkindale, Jane; Mishkind, Michael; Vierling, Elizabeth

doi:10.1002/9780470988503.ch5

Cited by 73 publications

(76 citation statements)

References 231 publications

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“…Mutants were chosen on the basis of previous data implicating the mutant gene in responses to high temperature (Table I) and included mutants in signaling pathways, mutants with defects in the production of antioxidants, and other mutants with defects in genes previously associated with heat stress or heatinduced pathways (Larkindale et al, 2005). Of the 46 plants tested, the most significant phenotypes in both basal and acquired thermotolerance were seen in several ABA biosynthesis or signaling mutants, in plants unable to accumulate SA, in two mutants of respiratory burst oxidase homologs, and in the uvh6 mutant, which is defective in a DNA helicase.…”

Section: Discussionmentioning

confidence: 99%

“…Acquired thermotolerance is induced by a short acclimation period at moderately high (but survivable) temperatures or by treatment with other nonlethal stress prior to heat stress (Kapoor et al, 1990;Vierling, 1991;Flahaut et al, 1996;Burke et al, 2000;Hong and Vierling, 2000;Massie et al, 2003;Larkindale et al, 2005). The ability to withstand and to acclimate to supra-optimal temperatures results from both prevention of heat damage and repair of heat-sensitive components.…”

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confidence: 99%

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Heat Stress Phenotypes of Arabidopsis Mutants Implicate Multiple Signaling Pathways in the Acquisition of Thermotolerance

et al. 2005

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To investigate the importance of different processes to heat stress tolerance, 45 Arabidopsis (Arabidopsis thaliana) mutants and one transgenic line were tested for basal and acquired thermotolerance at different stages of growth. Plants tested were defective in signaling pathways (abscisic acid, salicylic acid, ethylene, and oxidative burst signaling) and in reactive oxygen metabolism (ascorbic acid or glutathione production, catalase) or had previously been found to have temperature-related phenotypes (e.g. fatty acid desaturase mutants, uvh6). Mutants were assessed for thermotolerance defects in seed germination, hypocotyl elongation, root growth, and seedling survival. To assess oxidative damage and alterations in the heat shock response, thiobarbituric acid reactive substances, heat shock protein 101, and small heat shock protein levels were determined. Fifteen mutants showed significant phenotypes. Abscisic acid (ABA) signaling mutants (abi1 and abi2) and the UV-sensitive mutant, uvh6, showed the strongest defects in acquired thermotolerance of root growth and seedling survival. Mutations in nicotinamide adenine dinucleotide phosphate oxidase homolog genes (atrbohB and D), ABA biosynthesis mutants (aba1, aba2, and aba3), and NahG transgenic lines (salicylic acid deficient) showed weaker defects. Ethylene signaling mutants (ein2 and etr1) and reactive oxygen metabolism mutants (vtc1, vtc2, npq1, and cad2) were more defective in basal than acquired thermotolerance, especially under high light. All mutants accumulated wild-type levels of heat shock protein 101 and small heat shock proteins. These data indicate that, separate from heat shock protein induction, ABA, active oxygen species, and salicylic acid pathways are involved in acquired thermotolerance and that UVH6 plays a significant role in temperature responses in addition to its role in UV stress.Plants and other organisms have both an inherent ability to survive exposure to temperatures above the optimal for growth (basal thermotolerance) and an ability to acquire tolerance to otherwise lethal heat stress (acquired thermotolerance). Acquired thermotolerance is induced by a short acclimation period at moderately high (but survivable) temperatures or by treatment with other nonlethal stress prior to heat stress (Kapoor et al., 1990;Vierling, 1991;Flahaut et al., 1996;Burke et al., 2000;Hong and Vierling, 2000;Massie et al., 2003;Larkindale et al., 2005). The ability to withstand and to acclimate to supra-optimal temperatures results from both prevention of heat damage and repair of heat-sensitive components. Organisms must also maintain metabolic homeostasis during stress or be able to reestablish homeostasis subsequent to the stress period. Although plants are frequently subjected to dramatic heating to above the optimal growth temperature, relatively little is known about the critical genes controlling either basal or acquired thermotolerance in plants.Heat stress has a complex impact on cell function, suggesting that many processes are involved in th...

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Section: Discussionmentioning

confidence: 99%

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Heat Stress Phenotypes of Arabidopsis Mutants Implicate Multiple Signaling Pathways in the Acquisition of Thermotolerance

et al. 2005

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“…We call this maintenance of acquired thermotolerance short HS memory; it is an active process that can be separated genetically from the acquisition of thermotolerance (Charng et al, 2006(Charng et al, , 2007Meiri and Breiman, 2009). Across all kingdoms, HS induces the expression of various types of heat shock proteins (HSPs) that protect cellular proteins from denaturation (Larkindale et al, 2005;Richter et al, 2010). Generally, HSP expression is activated by HEAT SHOCK TRANSCRIPTION FACTORs (HSFs), peaks early after HS, and declines within a day to base levels (Scharf et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Arabidopsis miR156 Regulates Tolerance to Recurring Environmental Stress through SPL Transcription Factors

et al. 2014

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Plants are sessile organisms that gauge stressful conditions to ensure survival and reproductive success. While plants in nature often encounter chronic or recurring stressful conditions, the strategies to cope with those are poorly understood. Here, we demonstrate the involvement of ARGONAUTE1 and the microRNA pathway in the adaptation to recurring heat stress (HS memory) at the physiological and molecular level. We show that miR156 isoforms are highly induced after HS and are functionally important for HS memory. miR156 promotes sustained expression of HS-responsive genes and is critical only after HS, demonstrating that the effects of modulating miR156 on HS memory do not reflect preexisting developmental alterations. miR156 targets SPL transcription factor genes that are master regulators of developmental transitions. SPL genes are posttranscriptionally downregulated by miR156 after HS, and this is critical for HS memory. Altogether, the miR156-SPL module mediates the response to recurring HS in Arabidopsis thaliana and thus may serve to integrate stress responses with development.

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“…High temperatures disrupt the integrity of cellular membranes and cause changes in enzyme activity that lead to alterations in the rates of biochemical reactions and ultimately an imbalance in metabolic pathways (Berry and Björkman 1980;Levitt 1980;Larkindale et al 2005). The molecular basis of heat damage involves changes in protein conformation (Levitt 1980).…”

Section: Introductionmentioning

confidence: 99%

Heterologous expression of a plastid EF-Tu reduces protein thermal aggregation and enhances CO2 fixation in wheat (Triticum aestivum) following heat stress

Momčilović

Clemente

et al. 2008

Plant Mol Biol

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Heat stress is a major constraint to wheat production and negatively impacts grain quality, causing tremendous economic losses, and may become a more troublesome factor due to global warming. At the cellular level, heat stress causes denaturation and aggregation of proteins and injury to membranes leading to alterations in metabolic fluxes. Protein aggregation is irreversible, and protection of proteins from thermal aggregation is a strategy a cell uses to tolerate heat stress. Here we report on the development of transgenic wheat (Triticum aestivum) events, expressing a maize gene coding for plastidal protein synthesis elongation factor (EF-Tu), which, compared to non-transgenic plants, display reduced thermal aggregation of leaf proteins, reduced heat injury to photosynthetic membranes (thylakoids), and enhanced rate of CO 2 fixation after exposure to heat stress. The results support the concept that EF-Tu ameliorates negative effects of heat stress by acting as a molecular chaperone. This is the first demonstration of the introduction of a plastidal EF-Tu in plants that leads to protection against heat injury and enhanced photosynthesis after heat stress. This is also the first demonstration that a gene other than HSP gene can be used for improvement of heat tolerance and that the improvement is possible in a species that has a complex genome, hexaploid wheat. The results strongly suggest that heat tolerance of wheat, and possibly other crop plants, can be improved by modulating expression of plastidal EF-Tu and/or by selection of genotypes with increased endogenous levels of this protein.

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Plant Responses to High Temperature

Cited by 73 publications

References 231 publications

Heat Stress Phenotypes of Arabidopsis Mutants Implicate Multiple Signaling Pathways in the Acquisition of Thermotolerance

Heat Stress Phenotypes of Arabidopsis Mutants Implicate Multiple Signaling Pathways in the Acquisition of Thermotolerance

Arabidopsis miR156 Regulates Tolerance to Recurring Environmental Stress through SPL Transcription Factors

Heterologous expression of a plastid EF-Tu reduces protein thermal aggregation and enhances CO2 fixation in wheat (Triticum aestivum) following heat stress

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