Some like it hot, some like it warm: Phenotyping to explore thermotolerance diversity

Yeh, Chien-Hung; Kaplinsky, Nicholas J.; Hu, Catherine; Charng, Yee‐yung

doi:10.1016/j.plantsci.2012.06.004

Cited by 168 publications

(178 citation statements)

References 144 publications

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“…Thus, it is important to determine whether decreased fruit and seed set by heat stress is due to source or sink limitation. Unlike severe heat stress, moderate heat stress generally has no detrimental effect on photosynthesis (Lafta and Lorenzen, 1995;Yeh et al, 2012;Hancock et al, 2014). Consistently, we found that LMHS adopted in this study also had no effect on the leaf photosynthesis and total plant biomass in either wild-type or transgenic tomato (Supplemental Fig.…”

Section: Cwin Promotes Fruit Set Under Lmhs By Increasing Sink Strengsupporting

confidence: 84%

“…However, compared to SSHS, longterm moderate heat stress (LMHS) is a more frequent event under field conditions especially amid gradually increasing temperature associated with climate change (Sato et al, 2006). The response mechanisms of plants to LMHS may be drastically different from those to SSHS (Yeh et al, 2012;Hancock et al, 2014). For example, mitochondrial cochaperone MGE2 is required for the tolerance of Arabidopsis vegetative growth to LMHS (35°C for 9 d), but not for its response to SSHS (44°C for 150 min; Hu et al, 2012;Yeh et al, 2012).…”

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confidence: 99%

“…The response mechanisms of plants to LMHS may be drastically different from those to SSHS (Yeh et al, 2012;Hancock et al, 2014). For example, mitochondrial cochaperone MGE2 is required for the tolerance of Arabidopsis vegetative growth to LMHS (35°C for 9 d), but not for its response to SSHS (44°C for 150 min; Hu et al, 2012;Yeh et al, 2012). Despite its importance in developing strategies to improve crop adaptability to global warming, information on the effects of LMHS on plant development in general and on early reproductive development in particular remains scarce.…”

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confidence: 99%

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Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death

2016

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Reduced cell wall invertase (CWIN) activity has been shown to be associated with poor seed and fruit set under abiotic stress. Here, we examined whether genetically increasing native CWIN activity would sustain fruit set under long-term moderate heat stress (LMHS), an important factor limiting crop production, by using transgenic tomato (Solanum lycopersicum) with its CWIN inhibitor gene silenced and focusing on ovaries and fruits at 2 d before and after pollination, respectively. We found that the increase of CWIN activity suppressed LMHS-induced programmed cell death in fruits. Surprisingly, measurement of the contents of H 2 O 2 and malondialdehyde and the activities of a cohort of antioxidant enzymes revealed that the CWINmediated inhibition on programmed cell death is exerted in a reactive oxygen species-independent manner. Elevation of CWIN activity sustained Suc import into fruits and increased activities of hexokinase and fructokinase in the ovaries in response to LMHS. Compared to the wild type, the CWIN-elevated transgenic plants exhibited higher transcript levels of heat shock protein genes Hsp90 and Hsp100 in ovaries and HspII17.6 in fruits under LMHS, which corresponded to a lower transcript level of a negative auxin responsive factor IAA9 but a higher expression of the auxin biosynthesis gene ToFZY6 in fruits at 2 d after pollination. Collectively, the data indicate that CWIN enhances fruit set under LMHS through suppression of programmed cell death in a reactive oxygen species-independent manner that could involve enhanced Suc import and catabolism, HSP expression, and auxin response and biosynthesis.

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Section: Cwin Promotes Fruit Set Under Lmhs By Increasing Sink Strengsupporting

confidence: 84%

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confidence: 99%

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Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death

2016

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“…Understanding the roles of small RNAs in transcriptome homeostasis, cellular tolerance, phenological and developmental plasticity of plants under heat stress and recovery will help genetic engineering of stress tolerance in crop plants [90]. In addition, microarray technology has recently become a powerful tool for the systematic analysis of expression (or transcriptome) profiles of large numbers of genes those are induced or repressed by heat treatment [91,92]. Recent microarray studies in Arabidopsis deficient with APX gene, however, have found that certain HSPs are expressed typically under other stress conditions, although expression of HSPs under heat stress occurs normally [93].…”

Section: "Omics" Technologiesmentioning

confidence: 99%

Heat Stress Responses and Thermotolerance

Hemantaranjan¹,

Bhanu²,

Singh³

et al. 2014

APAR

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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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“…In the HSA32 null mutant of Arabidopsis, acquired thermotolerance is normally attained after a short recovery of 2 h, following heat acclimation treatment at 37°C for 1 h, but is significantly compromised after a long recovery for 48 h . Based on this phenotype, acquired thermotolerance attained after a long recovery period was named longterm acquired thermotolerance (LAT), as opposed to the ordinary short-term acquired thermotolerance (SAT; Yeh et al, 2012). The heat-inducible heat shock transcription factor HSFA2 and a peptidyl-prolyl cis-transisomerase (ROF1) have also been shown to be involved in LAT but not SAT (Charng et al, 2007;Meiri and Breiman, 2009).…”

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confidence: 99%

Interplay between Heat Shock Proteins HSP101 and HSA32 Prolongs Heat Acclimation Memory Posttranscriptionally in Arabidopsis

Juan

Hsu

et al. 2013

Plant Physiology

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Heat acclimation improves the tolerance of organisms to severe heat stress. Our previous work showed that in Arabidopsis (Arabidopsis thaliana), the "memory" of heat acclimation treatment decayed faster in the absence of the heat-stress-associated 32-kD protein HSA32, a heat-induced protein predominantly found in plants. The HSA32 null mutant attains normal short-term acquired thermotolerance but is defective in long-term acquired thermotolerance. To further explore this phenomenon, we isolated Arabidopsis defective in long-term acquired thermotolerance (dlt) mutants using a forward genetic screen. Two recessive missense alleles, dlt1-1 and dlt1-2, encode the molecular chaperone heat shock protein101 (HSP101). Results of immunoblot analyses suggest that HSP101 enhances the translation of HSA32 during recovery after heat treatment, and in turn, HSA32 retards the decay of HSP101. The dlt1-1 mutation has little effect on HSP101 chaperone activity and thermotolerance function but compromises the regulation of HSA32. In contrast, dlt1-2 impairs the chaperone activity and thermotolerance function of HSP101 but not the regulation of HSA32. These results suggest that HSP101 has a dual function, which could be decoupled by the mutations. Pulse-chase analysis showed that HSP101 degraded faster in the absence of HSA32. The autophagic proteolysis inhibitor E-64d, but not the proteasome inhibitor MG132, inhibited the degradation of HSP101. Ectopic expression of HSA32 confirmed its effect on the decay of HSP101 at the posttranscriptional level and showed that HSA32 was not sufficient to confer long-term acquired thermotolerance when the HSP101 level was low. Taken together, we propose that a positive feedback loop between HSP101 and HSA32 at the protein level is a novel mechanism for prolonging the memory of heat acclimation.

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Some like it hot, some like it warm: Phenotyping to explore thermotolerance diversity

Cited by 168 publications

References 144 publications

Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death

Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death

Heat Stress Responses and Thermotolerance

Interplay between Heat Shock Proteins HSP101 and HSA32 Prolongs Heat Acclimation Memory Posttranscriptionally in Arabidopsis

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