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Heat stress response (HSR) is a conserved mechanism developed to increase the expression of heat shock proteins (HSPs) via a heat shock factor (HSF)-dependent mechanism. Signaling by the stress phytohormone abscisic acid (ABA) is involved in acquired thermotolerance as well. Analysis of Arabidopsis (Arabidopsis thaliana) microarray databases revealed that the expression of HSFA6b, a class A HSF , extensively increased with salinity, osmotic, and cold stresses, but not heat. Here, we show that HSFA6b plays a pivotal role in the response to ABA and in thermotolerance. Salt-inducible HSFA6b expression was down-regulated in ABA-insensitive and -deficient mutants; however, exogenous ABA application restored expression in ABA-deficient, but not -insensitive plants. Thus, ABA signaling is required for proper HSFA6b expression. A transcriptional activation assay of protoplasts revealed that ABA treatment and coexpression of an ABA signaling master effector, ABA-RESPONSIVE ELEMENT-BINDING PROTEIN1, could activate the HSFA6b promoter. In addition, HSFA6b directly bound to the promoter of DEHYDRATION-RESPONSIVE ELEMENT-BINDING PROTEIN2A and enhanced its expression. Analysis of ABA responses in seed germination, cotyledon greening, and root growth as well as salt and drought tolerance in HSFA6b-null, overexpression, and dominant negative mutants revealed that HSFA6b is a positive regulator participating in ABA-mediated salt and drought resistance. Thermoprotection tests showed that HSFA6b was required for thermotolerance acquisition. Our study reveals a network in which HSFA6b operates as a downstream regulator of the ABA-mediated stress response and is required for heat stress resistance. This new ABA-signaling pathway is integrated into the complex HSR network in planta.

Ocean warming threatens corals and the coral reef ecosystem. Nevertheless, corals can be adapted to their thermal environment and inherit heat tolerance across generations. In addition, the diverse microbes that associate with corals have the capacity for more rapid change, potentially aiding the adaptation of long-lived corals. Here, we show that the microbiome of reef corals is different across thermally variable habitats and changes over time when corals are reciprocally transplanted. Exposing these corals to thermal bleaching conditions changes the microbiome for heat-sensitive corals, but not for heat-tolerant corals growing in habitats with natural high heat extremes. Importantly, particular bacterial taxa predict the coral host response in a short-term heat stress experiment. Such associations could result from parallel responses of the coral and the microbial community to living at high natural temperatures. A competing hypothesis is that the microbial community and coral heat tolerance are causally linked. Coral-associated microbes could enhance the capacity of their host organism to respond to environmental change. Ziegler and colleagues use a reciprocal transplant experiment to show that microbiomes of heat-tolerant corals are more resilient to change than those of heat-sensitive corals.

Understanding how species’ thermal limits have evolved across the tree of life is central to predicting species’ responses to climate change. Here, using experimentally-derived estimates of thermal tolerance limits for over 2000 terrestrial and aquatic species, we show that most of the variation in thermal tolerance can be attributed to a combination of adaptation to current climatic extremes, and the existence of evolutionary ‘attractors’ that reflect either boundaries or optima in thermal tolerance limits. Our results also reveal deep-time climate legacies in ectotherms, whereby orders that originated in cold paleoclimates have presently lower cold tolerance limits than those with warm thermal ancestry. Conversely, heat tolerance appears unrelated to climate ancestry. Cold tolerance has evolved more quickly than heat tolerance in endotherms and ectotherms. If the past tempo of evolution for upper thermal limits continues, adaptive responses in thermal limits will have limited potential to rescue the large majority of species given the unprecedented rate of contemporary climate change. Historical climate adaptation can give insight into the potential for adaptation to contemporary changing climates. Here Bennett et al. investigate thermal tolerance evolution across much of the tree of life and find different effects of ancestral climate on the subsequent evolution of ectotherms vs. endotherms.

Forecasting which species/ecosystems are most vulnerable to climate warming is essential to guide conservation strategies to minimize extinction. Tropical/mid-latitude species are predicted to be most at risk as they live close to their upper critical thermal limits (CTLs). However, these assessments assume that upper CTL estimates, such as CTmax, are accurate predictors of vulnerability and ignore the potential for evolution to ameliorate temperature increases. Here, we use experimental evolution to assess extinction risk and adaptation in tropical and widespread Drosophila species. We find tropical species succumb to extinction before widespread species. Male fertility thermal limits, which are much lower than CTmax, are better predictors of species’ current distributions and extinction in the laboratory. We find little evidence of adaptive responses to warming in any species. These results suggest that species are living closer to their upper thermal limits than currently presumed and evolution/plasticity are unlikely to rescue populations from extinction. Trait-based approaches assume upper critical thermal limits (CTLs) are good predictors of climate change vulnerability. Here, the authors show that male fertility thermal limits, which are lower than CTLs, are better at predicting Drosophila extinction in the lab, suggesting species may be living close to their thermal limits.

Background Exercise performance and capacity are impaired in hot, compared to temperate, conditions. Heat adaptation (HA) is one intervention commonly adopted to reduce this impairment because it may induce beneficial exercise performance and physiological and perceptual adaptations. A number of investigations have been conducted on HA but, due to large methodological differences, the effectiveness of different HA regimens remain unclear. Objectives (1) To quantify the effect of different HA regimens on exercise performance and the physiological and perceptual responses to subsequent heat exposure. (2) To offer practical HA recommendations and suggestions for future HA research based upon a systematic and quantitative synthesis of the literature. Data Source PubMed was searched for original research articles published up to, and including, 16 February 2016 using appropriate first- and second-order search terms. Study Selection English-language, peer-reviewed, full-text original articles using human participants were reviewed using the four-stage process identified in the PRISMA statement. Data Extraction Data for the following variables were obtained from the manuscripts by at least two of the authors: participant sex, maximal oxygen consumption and age; HA duration, frequency, modality, temperature and humidity; exercise performance and capacity; core and skin temperature; heart rate, stroke volume, cardiac output, skin blood flow, sweat onset temperature, body mass loss, sweat rate, perception of thirst, volitional fluid consumption, plasma volume changes; sweat concentrations of sodium, chloride and potassium; aldosterone, arginine vasopressin, heat shock proteins (Hsp), ratings of perceived exertion (RPE) and thermal sensation. Data Grouping Data were divided into three groups based upon the frequency of the HA regimen. Performance and capacity data were also divided into groups based upon the type of HA used. Data Analyses Hedges’ g effect sizes and 95 % confidence intervals were calculated. Correlations were run where appropriate. Results Ninety-six articles were reviewed. The most common duration was 7–14 days and the most common method of HA was the controlled work-rate approach. HA had a moderately beneficial effect on exercise capacity and performance in the heat irrespective of regimen; however, longer regimens were more effective than shorter approaches. HA had a moderate-to-large beneficial effect on lowering core body temperature before and during exercise, maintaining cardiovascular stability, and improving heat-loss pathways. Data are limited but HA may reduce oxygen consumption during subsequent exercise, improve glycogen sparing, increase the power output at lactate threshold, reduce lactate concentrations during exercise, have a trivial effect on increasing extracellular concentrations of Hsp, and improve perceived ratings of exertion and thermal sensation. Conclusion HA regimens lasting <14 days induce many beneficial physiological and perceptual adaptations to high ambient temperatures, and improve subsequent exercise performance and capacity in the heat; however, the extent of the adaptations is greatest when HA regimens lasting longer than 14 days are adopted. Large methodological differences in the HA literature mean that there is still uncertainty regarding the magnitude and time course of potential adaptation for a number of physiological and perceptual variables.

Although much is known about plant responses to heat shock (HS), how plants sense high temperature and the primary HS signal transduction pathway leading to HS-regulated gene expression are still poorly understood. To identify primary transcription factors that mediate HS-regulated gene expression and their target genes, RNA sequencing was performed to detect genes whose expression is rapidly altered by HS in Arabidopsis (Arabidopsis thaliana). The results showed several genes were induced after only 5 min of HS treatment, suggesting that HS signaling occurs very rapidly. Analysis of the cis-elements in the promoters of genes upregulated by 10 min of HS treatment identified HEAT SHOCK FACTOR A1s (HSFA1s) and circadian clock proteins REVEILLE4 (RVE4) and RVE8 as essential transcription factors that independently mediate early HS-induced gene expression. Using hsfa1a/b/d/e and rve4/8 mutants, we identified subsets of HSFA1s- or RVE4/8-dependent early HS-induced genes and showed RVE4/8 regulate plant thermotolerance partially by regulating the expression of downstream transcription factors ETHYLENE RESPONSIVE FACTOR53 (ERF53) and ERF54, specifically around noon. These findings reveal a potential transcriptional regulatory hierarchy governing the first wave of HS-induced gene expression. They also provided important insight into the mechanism by which the circadian clock gates thermotolerance and prepares plants for exposure to high temperatures during the day.

The wings of Lepidoptera contain a matrix of living cells whose function requires appropriate temperatures. However, given their small thermal capacity, wings can overheat rapidly in the sun. Here we analyze butterfly wings across a wide range of simulated environmental conditions, and find that regions containing living cells are maintained at cooler temperatures. Diverse scale nanostructures and non-uniform cuticle thicknesses create a heterogeneous distribution of radiative cooling that selectively reduces the temperature of structures such as wing veins and androconial organs. These tissues are supplied by circulatory, neural and tracheal systems throughout the adult lifetime, indicating that the insect wing is a dynamic, living structure. Behavioral assays show that butterflies use wings to sense visible and infrared radiation, responding with specialized behaviors to prevent overheating of their wings. Our work highlights the physiological importance of wing temperature and how it is exquisitely regulated by structural and behavioral adaptations. Butterfly wings have low thermal capacity and thus are vulnerable to damage by overheating. Here, Tsai et al. take an interdisciplinary approach to reveal the organs, nanostructures and behaviors that enable butterflies to sense and regulate their wing temperature.

Plants exposed to incidences of excessive temperatures activate heat-stress responses to cope with the physiological challenge and stimulate long-term acclimation 1 , 2 . The mechanism that senses cellular temperature for inducing thermotolerance is still unclear 3 . Here we show that TWA1 is a temperature-sensing transcriptional co-regulator that is needed for basal and acquired thermotolerance in Arabidopsis thaliana . At elevated temperatures, TWA1 changes its conformation and allows physical interaction with JASMONATE-ASSOCIATED MYC-LIKE (JAM) transcription factors and TOPLESS (TPL) and TOPLESS-RELATED (TPR) proteins for repressor complex assembly. TWA1 is a predicted intrinsically disordered protein that has a key thermosensory role functioning through an amino-terminal highly variable region. At elevated temperatures, TWA1 accumulates in nuclear subdomains, and physical interactions with JAM2 and TPL appear to be restricted to these nuclear subdomains. The transcriptional upregulation of the heat shock transcription factor A2 (HSFA2) and heat shock proteins depended on TWA1, and TWA1 orthologues provided different temperature thresholds, consistent with the sensor function in early signalling of heat stress. The identification of the plant thermosensors offers a molecular tool for adjusting thermal acclimation responses of crops by breeding and biotechnology, and a sensitive temperature switch for thermogenetics. TWA1 is a temperature-sensing transcriptional co-regulator that is needed for basal and acquired thermotolerance in Arabidopsis thaliana.

Key messageWe 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.

The thermal limit of ectotherms provides an estimate of vulnerability to climate change. It differs between contrasting microhabitats, consistent with thermal ecology predictions that a species’ temperature sensitivity matches the microclimate it experiences. However, observed thermal limits may differ between ectotherms from the same environment, challenging this theory. We resolved this apparent paradox by showing that ectotherm activity generates microclimatic deviations large enough to account for differences in thermal limits between species from the same microhabitat. We studied upper lethal temperature, effect of feeding mode on plant gas exchange, and temperature of attacked leaves in a community of six arthropod species feeding on apple leaves. Thermal limits differed by up to 8 °C among the species. Species that caused an increase in leaf transpiration (+182%), thus cooling the leaf, had a lower thermal limit than those that decreased leaf transpiration (−75%), causing the leaf to warm up. Therefore, cryptic microclimatic variations at the scale of a single leaf determine the thermal limit in this community of herbivores. We investigated the consequences of these changes in plant transpiration induced by plant–insect feedbacks for species vulnerability to thermal extremes. Warming tolerance was similar between species, at ±2 °C, providing little margin for resisting increasingly frequent and intense heat waves. The thermal safety margin (the difference between thermal limit and temperature) was greatly overestimated when air temperature or intact leaf temperature was erroneously used. We conclude that feedback processes define the vulnerability of species in the phyllosphere, and beyond, to thermal extremes.