Heat Stress Acclimation Research Articles

Integrated transcriptomic and proteomic analysis unravels the response mechanisms of Saccharina japonica to heat stress

High temperature is a major abiotic stress that limits the growth and productivity of seaweed. Over the past decades, the cold-temperate seaweed Saccharina japonica has been domesticated and gradually adapted to subtropical regions with higher temperatures. However, there is limited knowledge regarding the molecular responses of S. japonica to heat stress. In this study, an integrated transcriptomic and proteomic analysis was performed to explore the molecular mechanism underlying the response to heat stress in S. japonica. A total of 6777 genes and 226 proteins were identified that exhibited differential expression in heat stress samples comparison to non-stress sample. GO analysis revealed that the GO molecular function (MF) terms related to unfolded protein binding/protein binding, and heat shock protein (HSP) binding/HSP90 binding were significantly enriched in the up-regulated DEGs/DEPs in S. japonica sporophytes under heat stress. Further analysis of the global gene and protein expression profiles unveiled the potential mechanisms in S. japonica to alleviate heat stress through up-regulation of the heat stress transcription factor-heat shock proteins-HSP70/HSP90 organising proteins (HSF-HSPs-HOPs) module, down-regulation of reactive oxygen species (ROS) generation and up-regulation of ROS scavenging. Our results provide novel insights into the heat stress acclimation mechanism in S. japonica, and would benefit future selection of heat-tolerant varieties.

Proteomic Changes during Human Heat Stress and Heat Acclimation

INTRODUCTION. To thrive in a warmer climate, humans will need to adapt physiologically. Improved thermoregulatory and cardiovascular responses during heat acclimation have been widely described. However, the cellular and molecular mechanisms mediating these improvements remain understudied in humans. The aim of this study was to perform a broad-spectrum, non-targeted proteomic analysis to determine how plasma protein levels change in response to moderate heat stress and heat acclimation. METHODS. Ten healthy adults (4F/6H, age: 25 ± 3 years) attended two laboratory visits performed before and after a 7-day heat acclimation protocol (hot water immersion, 60 min at a rectal temperature ≥38.5°C). During the visits, blood samples were drawn before and during passive heat stress (~1.5°C increase in esophageal temperature, water-perfused suit). Proteomic analyses were performed on 2938 plasma proteins using the Olink Explore 3072 assay. We quantified the number of proteins that changed by more than one log2(fold change) in concentration. RESULTS. Prior to acclimation, ~1% of the proteins (n=29) changed in concentration during heat stress. The change in concentration for 9 of these proteins reached the p value threshold. After acclimation, 54 proteins changed in concentration under a normothermic state. During subsequent heat stress, 175 proteins (~6%) increased in concentration and 19 (~0.6%) decreased. For 180 of these proteins, the change in concentration during heat stress was unique to the post-acclimation visit. The genes for proteins that changed in concentration during heat stress prior to acclimation are more highly expressed in brain (FGFBP3), arterial (TIMP4), skin (OBP2B), lung/salivary gland/esophageal (CXCL17) tissue. The genes for proteins that changed concentration in response to heat acclimation are highly expressed in skin (MMP7, CA6, KLK14) and brain tissue (DNER). The genes for proteins that only changed in concentration during heat stress post-acclimation are more highly expressed in brain (MOG, SMOC1, PTPRN2), and arterial (TNC, C1QTNF1, MATN2, NTF3, SMOC1) tissue. CONCLUSION. This untargeted and large-scale proteomic analysis identified novel plasma proteins that change in concentration during human heat stress and subsequent heat acclimation. The individual protein results can be utilized as external validation for other studies, as the basis of further data analysis explorations, and/or to guide targeted investigations of the biological responses and adaptations to heat exposure. Natural Sciences and Engineering Research Council of Canada. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Multi-scale analysis of heat stress acclimation in Arabidopsis seedlings highlights the primordial contribution of energy-transducing organelles.

Much progress has been made in understanding the molecular mechanisms of plant adaptation to heat stress. However, the great diversity of models and stress conditions, and the fact that analyses are often limited to a small number of approaches, complicate the picture. We took advantage of a liquid culture system in which Arabidopsis seedlings are arrested in their development, thus avoiding interference with development and drought stress responses, to investigate through an integrative approach seedlings' global response to heat stress and acclimation. Seedlings perfectly tolerate a noxious heat shock (43°C) when subjected to a heat priming treatment at a lower temperature (38°C) the day before, displaying a thermotolerance comparable to that previously observed for Arabidopsis. A major effect of the pre-treatment was to partially protect energy metabolism under heat shock and favor its subsequent rapid recovery, which was correlated with the survival of seedlings. Rapid recovery of actin cytoskeleton and mitochondrial dynamics were another landmark of heat shock tolerance. The omics confirmed the role of the ubiquitous heat shock response actors but also revealed specific or overlapping responses to priming, heat shock, and their combination. Since only a few components or functions of chloroplast and mitochondria were highlighted in these analyses, the preservation and rapid recovery of their bioenergetic roles upon acute heat stress do not require extensive remodeling of the organelles. Protection of these organelles is rather integrated into the overall heat shock response, thus allowing them to provide the energy required to elaborate other cellular responses toward acclimation.

Multiomics analyses reveal the central role of the nucleolus and its machinery during heat stress acclimation in Pinus radiata.

Global warming is causing rapid changes in mean annual temperature and more severe drought periods. These are major contributors of forest dieback, which is becoming more frequent and widespread. In this work, we investigated how the transcriptome of Pinus radiata changed during initial heat stress response and acclimation. To this end, we generated a high-density dataset employing Illumina technology. This approach allowed us to reconstruct a needle transcriptome, defining 12 164 and 13 590 transcripts as down- and up-regulated, respectively, during a time course stress acclimation experiment. Additionally, the combination of transcriptome data with other available omics layers allowed us to determine the complex inter-related processes involved in the heat stress response from the molecular to the physiological level. Nucleolus and nucleoid activities seem to be a central core in the acclimating process, producing specific RNA isoforms and other essential elements for anterograde-retrograde stress signaling such as NAC proteins (Pra_vml_051671_1 and Pra_vml_055001_5) or helicase RVB. These mechanisms are connected by elements already known in heat stress response (redox, heat-shock proteins, or abscisic acid-related) and with others whose involvement is not so well defined such as shikimate-related, brassinosteriods, or proline proteases together with their potential regulatory elements. This work provides a first in-depth overview about molecular mechanisms underlying the heat stress response and acclimation in P. radiata.

A dataset of proteomic changes during human heat stress and heat acclimation

Hotter climates have important impacts on human health and performance. Yet, the cellular and molecular responses involved in human heat stress and acclimation remain understudied. This dataset includes physiological measurements and the plasma concentration of 2,938 proteins collected from 10 healthy adults, before and during passive heat stress that was performed both prior to and after a 7-day heat acclimation protocol. Physiological measurements included body temperatures, sweat rate, cutaneous vascular conductance, blood pressure, and skin sympathetic nerve activity. The proteomic dataset was generated using the Olink Explore 3072 assay, enabling a high-multiplex antibody-based assessment of protein changes based on proximity extension assay technology. The data need to be interpreted in the context of the moderate level of body hyperthermia attained and the specific demographic of young, healthy adults. We have made this dataset publicly available to facilitate research into the cellular and molecular mechanisms involved in human heat stress and acclimation, crucial for addressing the health and performance challenges posed by rising temperatures.

Melatonin influences methyl jasmonate-induced protection of photosynthetic activity in wheat plants against heat stress by regulating ethylene-synthesis genes and antioxidant metabolism

Melatonin (MT) and methyl jasmonate (MeJA) play important roles in the adaptation of plants to different stress factors by modulating stress tolerance mechanisms. The present study reports the involvement of MT (100 µM) in MeJA (10 µM)-induced photosynthetic performance and heat stress acclimation through regulation of the antioxidant metabolism and ethylene production in wheat (Triticum aestivum L.) plants. Plants exposed to 40 °C for 6 h per day for 15 days and allowed to retrieve at 28 °C showed enhanced oxidative stress and antioxidant metabolism, increased 1-aminocyclopropane-1-carboxylic acid (ACC) synthase (ACS) activity and ethylene production, and decreased photosynthetic performance. In contrast, the exogenously applied MT and MeJA reduced oxidative stress through improved S-assimilation (+ 73.6% S content), antioxidant defense system (+ 70.9% SOD, + 115.8% APX and + 104.2% GR, and + 49.5% GSH), optimized ethylene level to 58.4% resulting in improved photosynthesis by 75%. The use of p-chlorophenyl alanine, a MT biosynthesis inhibitor along with MeJA in the presence of heat stress reduced the photosynthetic performance, ATP-S activity and GSH content, substantiated the requirement of MT in the MeJA-induced photosynthetic response of plants under heat stress. These findings suggest that MeJA evoked the plant’s ability to withstand heat stress by regulating the S-assimilation, antioxidant defense system, and ethylene production, and improving photosynthetic performance was dependent on MT.

Arabidopsis HOT3/eIF5B1 constrains rRNA RNAi by facilitating 18S rRNA maturation

Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S ribosomal RNA (rRNA) 3' end maturation during late-stage 40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the genome-wide effects of eIF5B have not been studied at the single-nucleotide resolution in any organism, and 18S rRNA 3' end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3' end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3' end maturation or metabolism. We quantitatively defined processing hotspots and identified adenylation as the prevalent nontemplated RNA addition at the 3' ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNA interference to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3' portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions and were not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late 40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, messenger RNA (mRNA) translation initiation, and siRNA biogenesis in plants.

Impact of passive heat stress and passive heat acclimation on circulating extracellular vesicles: An exploratory analysis.

What is the central question of this study? How does passive heat stress and subsequent heat acclimation affect the circulating concentration of extracellular vesicles? What is the main finding and its importance? Passive heat stress increased the circulating concentration of total and platelet extracellular vesicles. Seven days of hot water immersion did not modify the change in circulating concentrations of extracellular vesicles during passive heat stress. This retrospective exploratory analysis aimed to improve our understanding of the effect of passive heat stress and subsequent heat acclimation on the circulating concentration of extracellular vesicles (EVs). Healthy young adults (four females and six males, 25±4 years of age, 1.72±0.08m in height and weighing 71.6±9.0kg) were heated with a water-perfused suit before and after seven consecutive days of hot water immersion. Pre-acclimation, participants were heated until oesophageal temperature increased to ∼1.4°C above baseline values. Post-acclimation, participants were heated until oesophageal temperature reached the same absolute value as the pre-acclimation visit (∼38.2°C). Venous blood samples were obtained before and at the end of passive heating to quantify plasma concentrations of EVs from all cell types (CSFE+ ), all cell types except erythrocytes (CSFE+ MHCI+ ), platelets (CSFE+ MHCI+ CD41+ ), endothelial cells (CSFE+ MHCI+ CD62e+ ), red blood cells (CSFE+ CD235a+ ) and leucocytes (CSFE+ MHCI+ CD45+ ) via flow cytometry. Passive heat stress increased the concentration of CFSE+ EVs (46,150,000/ml [3,620,784, 88,679,216], P=0.036), CFSE+ MHCI+ EVs (28,787,500/ml [9,851,127, 47,723,873], P=0.021) and CSFE+ MHCI+ CD41+ EVs (28,343,500/ml [9,637,432, 47,049,568], P=0.008). The concentration of CSFE+ MHCI+ CD62e+ EVs (94,230/ml [-55,099, 243,559], P=0.187), CSFE+ CD235a+ EVs (-1,414/ml [-15,709, 12,882], P=0.403) or CSFE+ MHCI+ CD45+ EVs (-192,915/ml [-690,166, 304,336], P=0.828) did not differ during heat stress. The change in circulating EVs during passive heat stress did not differ after heat acclimation (thermal state × acclimation interactions, all P≥0.180). These results demonstrate that passive heat stress increases the circulating concentration of total and platelet EVs and that passive heat acclimation does not alter this increase.

Nitric Oxide and Salicylic Acid Regulate Glutathione and Ethylene Production to Enhance Heat Stress Acclimation in Wheat Involving Sulfur Assimilation.

Phytohormones have a role in stress adaptation. The major mechanism underlying the role of exogenously-sourced nitric oxide (NO; as sodium nitroprusside, SNP: 50.0 µM) and salicylic acid (SA; 0.5 mM) in the presence of 2.0 mM SO4-2 was assessed in heat stress (HS; 40 °C for 6 h daily for 15 days) tolerance in wheat (Triticum aestivum L. cv. HD-3226). The cultivar HD-3226 possessed high photosynthetic sulfur use efficiency (p-SUE) among the six cultivars screened. Plants grown under HS exhibited an increased content of reactive oxygen species (ROS; including superoxide radical and hydrogen peroxide) and extent of lipid peroxidation with a consequent reduction in photosynthesis and growth. However, both NO and SA were found to be protective against HS via enhanced S assimilation. Their application reduced oxidative stress and increased the activity of antioxidant enzymes. NO or SA supplementation along with S under HS recovered the losses and improved photosynthesis and growth. The use of SA inhibitor (2-aminoindane-2-phosphonic acid; AIP) and NO scavenger (cPTIO) confirmed that the mitigating effects of SA and NO involved induction in S assimilation.

Small RNAs: The Essential Regulators in Plant Thermotolerance

Small RNAs (sRNAs) are a class of non-coding RNAs that consist of 21–24 nucleotides. They have been extensively investigated as critical regulators in a variety of biological processes in plants. sRNAs include two major classes: microRNAs (miRNAs) and small interfering RNAs (siRNAs), which differ in their biogenesis and functional pathways. Due to global warming, high-temperature stress has become one of the primary causes for crop loss worldwide. Recent studies have shown that sRNAs are involved in heat stress responses in plants and play essential roles in high-temperature acclimation. Genome-wide studies for heat-responsive sRNAs have been conducted in many plant species using high-throughput sequencing. The roles for these sRNAs in heat stress response were also unraveled subsequently in model plants and crops. Exploring how sRNAs regulate gene expression and their regulatory mechanisms will broaden our understanding of sRNAs in thermal stress responses of plant. Here, we highlight the roles of currently known miRNAs and siRNAs in heat stress responses and acclimation of plants. We also discuss the regulatory mechanisms of sRNAs and their targets that are responsive to heat stress, which will provide powerful molecular biological resources for engineering crops with improved thermotolerance.

Do thermal acclimation and an acute heat challenge alter myonuclear domain of control- and fast-growing quail?

Efforts to determine physiological traits that may render species resilient or susceptible to changing global temperatures have accelerated in recent years. Temperature is of critical importance to biological function; thus, climate change has the potential to severely affect all levels of biological organization in many species. For example, increases in environmental temperatures may alter muscle structure and function in birds. Myonuclear domain (MND), an under-studied aspect of avian muscle physiology that changes in response to thermal stress, is defined as the amount of cytoplasm within a muscle fiber that each nucleus is responsible for servicing. Here, we used two random bred lines of Japanese quail (Coturnix japonica) representing examples of control and fast growth rates. We used a factorial design to administer four treatment combinations to each line - an initial period of either heat-stress acclimation (Acclimation) or no acclimation (Not acclimated) followed by either a heat-stress challenge (HS) or no challenge (NC) after week 8 of age - to determine the effects of thermal acclimation and acute thermal stress on quail MND. We found a significant interaction between line * final treatment with fast-growing, HS birds demonstrating the lowest numbers of nuclei per mm of fiber, and Acclimated control-growing birds showing the highest numbers of nuclei per mm of fiber. There was a significant effect of line on MND with the fast-growing line having larger MNDs. Initial treatment with Not Acclimated birds showed larger MNDs. Additionally, control growing quail demonstrated positive correlations with fiber size, whereas fast growing quail did not. This may mean that nuclei in larger fibers of fast-growing quail may be functioning maximally, and that increases in temperature may also demonstrate similar effects.

Molecular mechanisms of plant tolerance to heat stress: current landscape and future perspectives.

We summarize recent studies focusing on the molecular basis of plant heat stress response (HSR), how HSR leads to thermotolerance, and promote plant adaptation to recurring heat stress events. The global crop productivity is facing unprecedented threats due to climate change as high temperature negatively influences plant growth and metabolism. Owing to their sessile nature, plants have developed complex signaling networks which enable them to perceive changes in ambient temperature. This in turn activates a suite of molecular changes that promote plant survival and reproduction under adverse conditions. Deciphering these mechanisms is an important task, as this could facilitate development of molecular markers, which could be ultimately used to breed thermotolerant crop cultivars. In current article, we summarize mechanisms involve in plant heat stress acclimation with special emphasis on advances related to heat stress perception, heat-induced signaling, heat stress-responsive gene expression and thermomemory that promote plant adaptation to short- and long-term-recurring heat-stress events. In the end, we will discuss impact of emerging technologies that could facilitate the development of heat stress-tolerant crop cultivars.

Role of Phytohormones in Regulating Heat Stress Acclimation in Agricultural Crops

Heat stress (HS) seriously affects crop growth, causing significant crop yield losses worldwide. The regulatory mechanisms controlling HS tolerance in plants are not well understood. Phytohormones are important molecules for coordinating myriad of phenomena related to plant growth and development. They are also essential endogenous signaling molecules that actively mediate numerous physiological responses under abiotic stress by triggering stress-responsive regulatory genes involved in plant growth. This review updates the central role of various phytohormones—indole acetic acid, gibberellic acid, abscisic acid, cytokinins, ethylene, salicylic acid, brassinosteroids, strigolactone, and jasmonic acid—in regulating the HS response so that plants can adapt to increasing temperature stress. We also reveal how these stress-responsive phytohormones switch on various regulatory gene(s) and genes encoding antioxidants and heat shock proteins (HSPs) to combat HS in various plant species.

Large geographic variability in the resistance of corals to thermal stress

AbstractAimPredictions for the future of coral reefs are largely based on thermal exposure and poorly account for potential geographic variation in biological sensitivity to thermal stress. Without accounting for complex sensitivity responses, simple climate exposure models and associated predictions may lead to poor estimates of future coral survival and lead to policies that fail to identify and implement the most appropriate interventions. To begin filling this gap, we evaluated a number of attributes of coral taxa and communities that are predicted to influence coral resistance to thermal stress over a large geographic range.LocationWestern Indo‐Pacific and Central Indo‐Pacific Ocean Realms.Major taxa studiedZooxanthellate Scleractinia – hard corals.MethodsWe evaluated the geographic variability of coral resistance to thermal stress as the ratio of thermal exposure and sensitivity in 12 countries during the 2016 global‐bleaching event. Thermal exposure was estimated by two metrics: (a) historical excess summer heat (cumulative thermal anomaly, CTA), and (b) a multivariate index of sea‐surface temperature (SST), light, and water flow (climate exposure, CE). Sensitivity was estimated for 226 sites using coordinated bleaching observations and underwater surveys of coral communities. We then evaluated coral resistance to thermal stress using 48 generalized linear mixed models (GLMMs) to compare the potential influences of geography, historical SST variation, coral cover and coral richness.ResultsGeographic faunal provinces and ecoregions were the strongest predictors of coral resistance to thermal stress, with sites in the Australian, Indonesian and Fiji‐Caroline Islands coral provinces having higher resistance to thermal stress than Africa‐India and Japan‐Vietnam provinces. Ecoregions also showed strong gradients in resistance with highest resistance to thermal stress in the western Pacific and Coral Triangle and lower resistance in the surrounding ecoregions. A more detailed evaluation of Coral Triangle and non‐Coral Triangle sites found higher resistance to thermal stress within the Coral Triangle, associated with c. 2.5 times more recent historical thermal anomalies and more centralized, warmer, and cool‐water skew SST distributions, than in non‐Coral Triangle sites. Our findings identify the importance of environmental history and geographic context in future predictions of bleaching, and identify some potential drivers of coral resistance to thermal stress.Main conclusionsSimple threshold models of heat stress and coral acclimation are commonly used to predict the future of coral reefs. Here and elsewhere we show that large‐scale responses of coral communities to heat stress are geographically variable and associated with differential environmental stresses and histories.

Recent Advances in Genetic and Epigenetic Modulation of Animal Exposure to High Temperature.

Animals have evolved multiple systems, including genetic and epigenetic systems, to respond accordingly to heat exposure and heat acclimation. Heat exposure greatly affects immunity, changes metabolic processes, and poses a serious threat to animals. Heat acclimation is induced by repeated organism exposure to heat stress to dissipate heat. This review focuses on genetic modulation via heat shock transcription factors and calcium as two important factors and compares the changes in HSPs under heat stress and heat acclimation. Epigenetic regulation summarizes the role of HSPs in DNA methylation and histone modifications under heat stress and heat acclimation. These genetic and epigenetic modifications protect cells from thermal damage by mediating the transcriptional levels of heat-responsive genes. This review highlights recent advances in the genetic and epigenetic control of animal thermal responses and their interactions.

Impact of passive heat acclimation on markers of kidney function during heat stress.

What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress. Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26±5 years of age; 72.7±8.6kg; 172.4±7.5cm) underwent passive heat stress before and after a 7day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133±41mlmin-1 ; post, 127±51mlmin-1 ; P=0.99) and after (pre, 129±46mlmin-1 ; post, 130±36mlmin-1 ; P=0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P<0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, -0.86±0.67mlmin-1 ; post, 0.40±1.01mlmin-1 ; P<0.01) but not after (pre, -0.16±0.57mlmin-1 ; post, 0.76±1.2mlmin-1 ; P=0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P<0.03) but not sodium (P=0.13) or chloride (P=0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58±51%; after, 8±29%; P=0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urine-concentrating ability and filtration within the glomerulus.

A defect in BRI1-EMS-SUPPRESSOR 1 (bes1)-mediated brassinosteroid signaling increases photoinhibition and photo-oxidative stress during heat stress in Arabidopsis

Heat stress has negative effects on plant performance, especially in photosynthesis and photoprotection. To withstand heat stress, plants modulate steroid phytohormones, brassinosteroids (BRs). However, their regulation and functions in heat stress acclimation are still poorly understood. Plant growth, photoinhibition, photo-oxidative stress and endogenous contents of hormones (including not only BRs but also abscisic acid, salicylic acid and jasmonic acid) were evaluated during heat stress in Arabidopsis thaliana wild type plants and loss-of-function mutations in either BR biosynthetic or signaling genes. It was found that a defect in BRI1-EMS-SUPPRESSOR 1 (bes1)-mediated BR signaling showed the most sensitive characteristics to heat stress compared to wild type and other BR mutants. Sensitivity was associated with declined PSII photochemistry efficiency (Fv/Fm) together with increased carotenoid, tocopherol and lipid hydroperoxide contents, which evidences higher photoinhibition and photo-oxidative stress in the bes1 mutant under heat stress. Furthermore, the bes1 mutant showed greater contents of abscisic acid (ABA) after one day of exposure to heat stress. However, all heat stress symptoms in the bes1 mutant could be mitigated by the application of 24-epibrassinolide. Therefore, it is concluded that BES1 transcription factor plays a role in plants responses to heat stress, relieving photoinhibition and photo-oxidative stress, but that alternative BR signaling pathways to BES1 may also be effective in heat stress acclimation. Furthermore, this study emphasizes the complex interplay between BR and ABA in the heat acclimation process.

Vitamin E Function in Stress Sensing and Signaling in Plants

Vitamin E is involved in heat stress acclimation. In this issue of Developmental Cell, Fang etal. (2018) uncover a new link between Vitamin E and plant retrograde signaling and show that vitamin E is required for the accumulation of 3'-phosphoadenosine 5'-phosphate, an inhibitor of exoribonucleases, to protect microRNAs from degradation.

Thermal acclimation of fast-growing Japanese Quails (Coturnix japonica) exhibit decreased oxidative stress and increased muscle fiber diameters after acute heat challenges

Many predict dire consequences of increasing temperatures; however, high temperatures in early life may aid animals during extreme thermal events later in life. The underlying physiological mechanisms have not been elucidated. We examined whether developing in warmer temperatures would physiologically benefit adult Japanese Quails (Coturnix japonica Temminck and Schlegel, 1849) by exploring changes in oxidative stress and muscle structure in two quail lines — one selected for control growth and another for fast growth and after acute heat challenges. We used a factorial design to administer four treatment combinations to each line: an initial period of either heat-stress acclimation (3 h every other day to 37 °C) or no acclimation, and after 5 weeks, either an acute heat-stress challenge (8 h at 39 °C) or no challenge. We found that control quails had significantly higher citrate synthase activity than fast-growing quails. Fast-growing quails had higher hydroxyl scavenging capacity than control quails. Peroxyl scavenging capacity decreased in both lines after an acute heat challenge, regardless of acclimation. Finally, fast-growing quails had larger muscle fiber diameters than control quails, and acclimated birds that experienced an acute heat challenge had larger muscle fibers than those that did not experience a heat challenge. Thus, fast-growing quails may physiologically benefit from developing in warmer temperatures.

Respiratory burst oxidase homologue-dependent H2 O2 and chloroplast H2 O2 are essential for the maintenance of acquired thermotolerance during recovery after acclimation.

Thermotolerance is improved by heat stress (HS) acclimation, and the thermotolerance level is "remembered" by plants. However, the underlying signalling mechanisms remain largely unknown. Here, we showed NADPH oxidase-mediated H2 O2 (NADPH-H2 O2 ), and chloroplast-H2 O2 promoted the sustained expression of HS-responsive genes and programmed cell death (PCD) genes, respectively, during recovery after HS acclimation. When spraying the NADPH oxidase inhibitor, diphenylene iodonium, after HS acclimation, the NADPH-H2 O2 level significantly decreased, resulting in a decrease in the expression of HS-responsive genes and the loss of maintenance of acquired thermotolerance (MAT). In contrast, compared with HS acclimation, NADPH-H2 O2 declined but chloroplast-H2 O2 further enhanced during recovery after HS over-acclimation, resulting in the reduced expression of HS-responsive genes and substantial production of PCD. Notably, the further inhibition of NADPH-H2 O2 after HS over-acclimation also inhibited chloroplast-H2 O2 , alleviating the severe PCD and surpassing the MAT of HS over-acclimation treatment. Due to the change in subcellular H2 O2 after HS acclimation, the tomato seedlings maintained a constant H2 O2 level during recovery, resulting in stable and lower total H2 O2 levels during a tester HS challenge conducted after recovery. We conclude that tomato seedlings increase their MAT by enhancing NADPH-H2 O2 content and controlling chloroplast-H2 O2 production during recovery, which enhances the expression of HS-responsive genes and balances PCD levels, respectively.