Acquisition Of Thermotolerance Research Articles

Arabidopsis HSFA9 Acts as a Regulator of Heat Response Gene Expression and the Acquisition of Thermotolerance and Seed Longevity.

Heat-shock transcription factors (HSFs) are crucial for regulating plant responses to heat and various stresses, as well as for maintaining normal cellular functions and plant development. HSFA9 and HSFA2 are two of the Arabidopsis class A HSFs and their expressions are dramatically induced in response to heat shock (HS) stress among all 21 Arabidopsis HSFs. However, the detailed biological roles of their cooperation have not been fully characterized. In this study, we employed an integrated approach that combined bioinformatics, molecular genetics and computational analysis to identify and validate the molecular mechanism that controls seed longevity and thermotolerance in Arabidopsis. The acquisition of tolerance to deterioration was accompanied by a significant transcriptional switch that involved the induction of primary metabolism, reactive oxygen species and unfolded protein response, as well as the regulation of genes involved in response to dehydration, heat and hypoxia. In addition, the cis-regulatory motif analysis in normal stored and controlled deterioration treatment (CDT) seeds confirmed the CDT-repressed genes with heat-shock element (HSE) in their promoters. Using a yeast two-hybrid and molecular dynamic interaction assay, it is shown that HSFA9 acted as a potential regulator that can interact with HSFA2. Moreover, the knock-out mutants of both HSFA9 and HSFA2 displayed a significant reduction in seed longevity. These novel findings link HSF transcription factors with seed deterioration tolerance and longevity.

Comparative analysis of genome-wide transcriptional responses to continuous heat stress in Pleurotus tuoliensis

Temperature plays an impactful role in mushroom cultivation. To obtain insights of transcriptomic response in macrofungi against heat stress, we performed RNA-seq analysis using Pleurotus tuoliensis mycelium cells that were treated under 32 °C and 36 °C for consecutive 96 h. By comparing the growth rate data, we found mycelium cells could maintain normal growth rate almost the same as control under 32 °C, yet halted the growths under 36 °C. In total, 2724 differential expressed genes were identified from the three pair-wise comparisons, which were classified to four clusters based on their expression patterns. We also performed gene set enrichment analysis using both GO and KEGG databases, and revealed 48, 113 and 105 enriched GO terms, and 1, 5, and 6 enriched KEGG pathways for three pair-wise comparisons accordingly. In addition, we identified 9 overlapping GO terms and 1 overlapping KEGG pathway shared by the three comparisons. Differentially expressed genes (DEGs) involved in cell communication, amino acid metabolic process, intracellular signal transduction and small molecule biosynthesis were identified in two heat stress treatments despite of the stress intensity. However, the expression of two heat shock protein genes (HSP10 and HSP60) were induced by increasing temperature. Our findings also suggested the DEGs associated with cell cycle regulation had various expression patterns under two heat stress conditions possibly due to different functions. Furthermore, 11 DEGs related to ergosterol biosynthesis were identified with similar expression trends, indicating the ergosterol levels and cell membrane composition may have a tight connection to the acquisition of thermotolerance, which warrant further investigations for deeper understanding of molecular mechanisms in fungal stress responses.

The cell functions of phospholipase C-1, Ca2+/H+ exchanger-1, and secretory phospholipase A2 in tolerance to stress conditions and cellulose degradation in Neurospora crassa.

We investigated the cell functions of the Ca2+ signaling genes phospholipase C-1 (plc-1), Ca2+/H+ exchanger (cpe-1), and secretory phospholipase A2 (splA2) for stress responses and cellulose utilization in Neurospora crassa. The Δplc-1, Δcpe-1, and ΔsplA2 mutants displayed increased sensitivity to the alkaline pH and reduced survival during induced thermotolerance. The ΔsplA2 mutant also exhibited hypersensitivity to the DTT-induced endoplasmic reticulum (ER) stress, increased microcrystalline cellulose utilization, increased protein secretion, and glucose accumulation in the culture supernatants. Moreover, the ΔsplA2 mutant could notgrow on microcrystalline cellulose during ER stress. Furthermore, plc-1, cpe-1, and splA2 synthetically regulate the acquisition of thermotolerance induced by heat shock, responses to alkaline pH and ER stress, and utilization of cellulose and other alternate carbon sources in N. crassa. In addition, expression of the alkaline pH regulator, pac-3, and heat shock proteins, hsp60, and hsp80 was reduced in the Δplc-1, Δcpe-1, and ΔsplA2 single and double mutants. The expression of the unfolded protein response (UPR) markers grp-78 and pdi-1 was also significantly reduced in the mutants showing growth defect during ER stress. The increased cellulolytic activities of the ΔsplA2 and Δcpe-1; ΔsplA2 mutants were due to increased cbh-1, cbh-2, and endo-2 expressionin N. crassa. Therefore, plc-1, cpe-1, and splA2 are involved in stress responses and cellulose utilizationin N. crassa.

Hepatic heat shock proteins, antioxidant-related genes, and immunocompetence of heat-stressed broilers in response to short periods of incubation during egg storage and thermal conditioning

Short Periods of Incubation During Egg Storage (SPIDES) approach improves chick quality and hatching rates. Also, embryonic thermal conditioning (TC) is a strategy for enhancing thermotolerance in avian species. Until now, evaluating the effect of either SPIDES or embryonic TC effects has only been separately conducted, so we hypothesized that combining TC and SPIDES may enhance the response of broilers to thermal stress. Eight hundred Ross broiler eggs were divided into two groups; the first one was kept under appropriate storage room conditions, S0 (control) The 2nd was subjected to SPIDES for 5 h at 37.8 ○C ± 0.1 three times at days 5, 10, and 15 (S1) after egg collection respectively. On the 14th day of incubation (DOI) each of the two main groups was randomly divided into two equal subgroups; the control one was left under the appropriate incubation settings (TC0) whereas the other received prenatal heat conditioning (TC1) at 39.5 ○C ± 0.1 for 6 h/d from the 14th to the 18th embryonic day (E), resulting finally in four experimental subgroups (S0TC0, S1TC0, S0TC1 & S1TC1). Resultsshowed that SPIDES treatment improved the hatchability of the stored eggs by almost 20% compared to untreated eggs. A combination of SPIDES and TC (S1TC1) increased significantly the levels of Immunoglobulin (IgG and IgM) production at hatch and heat-stressed birds. Our findings revealed that the hepatic heat shock proteins (hsp70, 90 A,90 B, 60 and hspA9), antioxidants-related genes (CAT, and SOD2), and NADPH4 were significantly downregulated in the thermally conditioned group that challenged with thermal stress conditions. As opposed to that, the SPIDES group showed a significant increase in hepatic heat shock proteins, antioxidants-related genes, and NADPH4 when subjected to thermal-stress conditions.In conclusion, the combination of SPIDES and TC has a positive effect on some pre and post-hatch traits of broiler chicks. Under heat stress challenge, thermal conditioning can modify the expression of antioxidant-related genes and Hsps, leading to the enhanced acquisition of thermotolerance as evidenced by lower expression of Hsps and NADPH4. While SPIDES does not have a significant role in thermotolerance acquisition.

Enhancing heat stress tolerance in Lanzhou lily (Lilium davidii var. unicolor) with Trichokonins isolated from Trichoderma longibrachiatum SMF2.

Lanzhou lily (Lilium davidii var. unicolor) is a renowned edible crop produced in China and relatively sensitive to high temperature (HT). Trichokonins (TKs) are antimicrobial peptaibols secreted from Trichoderma longibrachiatum strain SMF2. Here, we report that TKs application improves the thermotolerance of Lanzhou lily. The activity of the antioxidant enzyme system (SOD, CAT, and POD), the level of heat-resistance-associated phytohormones (ABA, SA, and JA), the relative water content (RWC), the content of chlorophyll (Chl), and the net photosynthetic rate (P n) were promoted by TKs treatment in Lanzhou lily plants subjected to heat stress (HS). TKs treatment also mitigated cell injury as shown by a lower accumulation of malondialdehyde (MDA) and relative electrolyte leakage (REL) under HS conditions. RNA-seq data analysis showed that more than 4.5 times differentially expressed genes (DEGs) responded to TKs treatment under HS compared to non-HS, and TKs treatment reduced protein folding and enhanced cellular repair function under HS conditions. The analyses of DEGs involved in hormone (ABA, SA and JA) synthesis and signaling pathways suggested that TKs might improve Lanzhou lily heat tolerance by promoting ABA synthesis and signal transduction. TKs highly induced DEGs of the HSF-HSP pathway under HS, in which HSFA2 accounted for most of the HSF family. Furthermore, TKs treatment resulted in the upregulation of heat-protective genes LzDREB2B, LzHsfA2a, LzMBF1c, LzHsp90, and LzHsp70 involved in HSF-HSP signal pathway after long-term HS. LzHsfA2a-1 likely plays a key role in acquisition of TKs-induced thermotolerance of Lanzhou lily as evidenced by the sustained response to HS, the enhanced response to TKs treatment under long-term HS, and the high sequence similarity to LlHsfA2a which is a key regulator for the improvement of heat tolerance in Lilium longiflorum. Our results reveal the underlying mechanisms of TKs-mediated thermotolerance in Lanzhou lily and highlight an attractive approach to protecting crop plants from damage caused by HS in a global warming future.

Chloroplast-localized GUN1 contributes to the acquisition of basal thermotolerance in Arabidopsis thaliana.

Heat stress (HS) severely affects different cellular compartments operating in metabolic processes and represents a critical threat to plant growth and yield. Chloroplasts are crucial for heat stress response (HSR), signaling to the nucleus the environmental challenge and adjusting metabolic and biosynthetic functions accordingly. GENOMES UNCOUPLED 1 (GUN1), a chloroplast-localized protein, has been recognized as one of the main players of chloroplast retrograde signaling. Here, we investigate HSR in Arabidopsis wild-type and gun1 plantlets subjected to 2 hours of HS at 45°C. In wild-type plants, Reactive Oxygen Species (ROS) accumulate promptly after HS, contributing to transiently oxidize the cellular environment and acting as signaling molecules. After 3 hours of physiological recovery at growth temperature (22°C), the induction of enzymatic and non-enzymatic antioxidants prevents oxidative damage. On the other hand, gun1 mutants fail to induce the oxidative burst immediately after HS and accumulate ROS and oxidative damage after 3 hours of recovery at 22°C, thus resulting in enhanced sensitivity to HS. These data suggest that GUN1 is required to oxidize the cellular environment, participating in the acquisition of basal thermotolerance through the redox-dependent plastid-to-nucleus communication.

Drought Stress Pre-Treatment Triggers Thermotolerance Acquisition in Durum Wheat

Durum wheat is strongly affected by climatic constraints such as high temperatures and drought, which frequently lead to yield reduction. Damages due to high temperatures are related to plant thermotolerance, a trait determined by two components: basal and acquired thermotolerance. In this study, the effect of drought and heat stress imposed singularly or sequentially was investigated in ten durum wheat cultivars (cvs) at the physiological and molecular level. The traits analyzed were cell membrane stability, relative water content, proline content, and expression level of several genes for heat shock proteins (HSPs). Our results indicate that drought priming can induce the acquisition of thermotolerance in most cultivars already classified as able to acquire thermotolerance by heat pre-treatment. Proline accumulation was correlated to cell membrane stability, meaning that the most thermotolerant cvs were able to accumulate higher levels of proline. Acquired thermotolerance is also due to the activation of HSP gene expression; similarly, pre-treatment with water stress was able to activate HSPs expression. The results reported indicate that water stress plays an important role in inducing thermotolerance, comparable to mild heat stress pre-treatment. This is the first report on the effect of drought stress on the acquisition of thermotolerance.

Thermomemory in shoot apical meristem: Regulation of carbohydrate metabolism and stem cell identity

Adaptation to the environment is essential for sessile organisms, such as plants, as they cannot move away from adverse conditions. Heat stress (HS) is one of the most serious environmental stresses in terms of its effect on crop growth and yield, especially in this era of global warming. Therefore, research on heat responses and acclimation in plants is becoming increasingly important. Plants have evolved complex systems to respond to HS for their survival. In general, heat shock transcription factors (Hsfs) are involved in the acquisition of thermotolerance, through regulation of the expression of genes encoding the heat shock proteins (HSPs) that function as molecular chaperones protecting cells from HS (von Koskull-Döring et al., 2007; Richter et al., 2010).

Modulating the Heat Stress Response to Improve Hyperthermia-Based Anticancer Treatments.

Simple SummaryHyperthermia is a method to expose a tumor to elevated temperatures. Heating of the tumor promotes the effects of various treatment regimens that are based on chemo and radiotherapy. Several aspects, however, limit the efficacy of hyperthermia-based treatments. This review provides an overview of the effects and limitations of hyperthermia and discusses how current drawbacks of the therapy can potentially be counteracted by inhibiting the heat stress response—a mechanism that cells activate to defend themselves against hyperthermia.Cancer treatments based on mild hyperthermia (39–43 °C, HT) are applied to a widening range of cancer types, but several factors limit their efficacy and slow down more widespread adoption. These factors include difficulties in adequate heat delivery, a short therapeutic window and the acquisition of thermotolerance by cancer cells. Here, we explore the biological effects of HT, the cellular responses to these effects and their clinically-relevant consequences. We then identify the heat stress response—the cellular defense mechanism that detects and counteracts the effects of heat—as one of the major forces limiting the efficacy of HT-based therapies and propose targeting this mechanism as a potentially universal strategy for improving their efficacy.

Grapevine Responses to Heat Stress and Global Warming

The potential effects of the forthcoming climate change include the rising of the average annual temperature and the accumulation of extreme weather events, like frequent and severe heatwaves, a phenomenon known as global warming. Temperature is an important environmental factor affecting almost all aspects of growth and development in plants. The grapevine (Vitis spp.) is quite sensitive to extreme temperatures. Over the current century, temperatures are projected to continue rising with negative impacts on viticulture. These consequences range from short-term effects on wine quality to long-term issues such as the suitability of certain varieties and the sustainability of viticulture in traditional wine regions. Many viticultural zones, particularly in Mediterranean climate regions, may not be suitable for growing winegrapes in the near future unless we develop heat-stress-adapted genotypes or identify and exploit stress-tolerant germplasm. Grapevines, like other plants, have developed strategies to maintain homeostasis and cope with high-temperature stress. These mechanisms include physiological adaptations and activation of signaling pathways and gene regulatory networks governing heat stress response and acquisition of thermotolerance. Here, we review the major impacts of global warming on grape phenology and viticulture and focus on the physiological and molecular responses of the grapevine to heat stress.

HOS1 activates DNA repair systems to enhance plant thermotolerance.

Plants possess an astonishing capability of effectively adapting to a wide range of temperatures, ranging from freezing to near-boiling temperatures1,2. Yet, heat is a critical obstacle to plant survival. The deleterious effects of heat shock on cell function include misfolding of cellular proteins, disruption of cytoskeletons and membranes, and disordering of RNA metabolism and genome integrity3-5. Plants stimulate diverse heat shock response pathways in response to abrupt temperature increases. While it is known that stressful high temperatures disturb genome integrity by causing nucleotide modifications and strand breakages or impeding DNA repair6, it is largely unexplored how plants cope with heat-induced DNA damages. Here, we demonstrated that high expression of osmotically reponsive genes 1 (HOS1) induces thermotolerance by activating DNA repair components. Thermotolerance and DNA repair capacity were substantially reduced in HOS1-deficient mutants, in which thermal induction of genes encoding DNA repair systems, such as the DNA helicase RECQ2, was markedly decreased. Notably, HOS1 proteins were thermostabilized in a heat shock factor A1/heat shock protein 90 (HSP90)-dependent manner. Our data indicate that the thermoresponsive HSP90-HOS1-RECQ2 module contributes to sustaining genome integrity during the acquisition of thermotolerance, providing a distinct molecular link between DNA repair and thermotolerance.

HIKESHI silencing can enhance mild hyperthermia sensitivity in human oral squamous cell carcinoma HSC‑3 cells.

Hyperthermia (HT) is considered to be of value as a treatment modality in various cancers. However, the acquisition of thermotolerance in cancer cells due to the induction of heat shock proteins (HSPs) makes HT less effective. Recent findings have indicated that heat shock protein nuclear import factor hikeshi (HIKESHI), also referred to as C11orf73, acts as a nuclear import carrier of Hsp70 under heat stress conditions. The aim of the present study was to determine whether knockdown (KD) of HIKESHI by small interfering RNA (siRNA) can potentiate mild HT (MHT) sensitivity in human oral squamous cell carcinoma (OSCC) HSC-3 cells. The mRNA and protein expression of HIKESHI was found to be markedly suppressed in HSC-3 cells treated with siRNA for HIKESHI (siHIKE). Silencing HIKESHI significantly decreased the cell viability under MHT conditions (42°C for 90 min). Immunocytochemical and western blot analyses clearly demonstrated that Hsp70 protein translocated from the cytoplasm to the nucleus under MHT conditions, and this translocation was significantly inhibited in cells treated with siHIKE. Treatment of the cells with MHT transiently increased the phosphorylation level of extracellular signal-regulated kinase (ERK)2. Furthermore, the phosphorylation was sustained in HIKESHI-KD cells under MHT conditions, and this sustained phosphorylation was abolished by pretreatment with U0126, an inhibitor of mitogen-activated protein kinase/ERK. In addition, U0126 significantly decreased the viability of cells treated with the combination of HIKESHI-KD and MHT. The data of the present study suggest that HIKESHI silencing enhanced the sensitivity of human OSCC HSC-3 cells to MHT.

HSF3 and Hsp70 Expression during Post-Hatch Cold Stress in Broiler Chickens Subjected to Embryonic Thermal Manipulation.

Decades of selective breeding for commercial purposes have rendered the broiler chicken (Gallus gallus domesticus) highly susceptible to heat and cold stress. A multitude of studies have documented the effects of thermal manipulation (TM) on broiler thermotolerance during periods of post-hatch heat stress, but very few have focused on the effect of TM on a broiler’s ability to withstand cold stress. Therefore, the primary objective of the current study is to determine the effects of TM on the acquisition of thermotolerance in broilers via their expression of the stress-associated 70 kilodalton heat shock protein (Hsp70) gene and heat shock factor 3 (HSF3) gene. Briefly, Hubbard broiler embryos were subject to TM by increasing the incubation temperature to 39 °C and 65% relative humidity (RH) for 18 h daily, from embryonic days (ED) 10 to 18. Broilers were then exposed to cold stress by decreasing the room temperature to 16 °C during post-hatch days 32 to 37. After thermal challenge, broilers were euthanized and hepatic and splenic tissues were collected. Our results showed that TM decreased the hatchability rate and body temperature but improved the body weight gain. TM generally decreased the hepatic expression but did not change the splenic expression of HSF3 during cold stress. In contrast, both hepatic and splenic Hsp70 expression decreased during cold stress. The results of the present study may suggest that TM significantly affects a broiler’s genetic response to cold stress.

Molecular mechanisms of acclimation to long-term elevated temperature exposure in marine symbioses.

Seawater temperature rise in French Polynesia has repeatedly resulted in the bleaching of corals and giant clams. Because giant clams possess distinctive ectosymbiotic features, they represent a unique and powerful model for comparing molecular pathways involved in (a) maintenance of symbiosis and (b) acquisition of thermotolerance among coral reef organisms. Herein, we explored the physiological and transcriptomic responses of the clam hosts and their photosynthetically active symbionts over a 65day experiment in which clams were exposed to either normal or environmentally relevant elevated seawater temperatures. Additionally, we used metabarcoding data coupled with in situ sampling/survey data to explore the relative importance of holobiont adaptation (i.e., a symbiont community shift) versus acclimation (i.e., physiological changes at the molecular level) in the clams' responses to environmental change. We finally compared transcriptomic data to publicly available genomic datasets for Symbiodiniaceae dinoflagellates (both cultured and in hospite with the coral Pocillopora damicornis) to better tease apart the responses of both hosts and specific symbiont genotypes in this mutualistic association. Gene module preservation analysis revealed that the function of the symbionts' photosystem II was impaired at high temperature, and this response was also found across all holobionts and Symbiodiniaceae lineages examined. Similarly, epigenetic modulation appeared to be a key response mechanism for symbionts in hospite with giant clams exposed to high temperatures, and such modulation was able to distinguish thermotolerant from thermosensitive Cladocopium goreaui ecotypes; epigenetic processes may, then, represent a promising research avenue for those interested in coral reef conservation in this era of changing global climate.

Dominant mutants of the calcineurin catalytic subunit (CNA-1) showed developmental defects, increased sensitivity to stress conditions, and CNA-1 interacts with CaM and CRZ-1 in Neurospora crassa.

We studied a dominant mutant of the Neurospora crassa calcineurin catalytic (cna-1) subunit generated using the repeat-induced point mutation (RIP). The Cna-1RIP mutants showed defects in morphology, aerial hyphae development, carotenoid accumulation, and fertility. The Cna-1RIP mutants also showed sensitivity to osmotic stress and a reduction in acquisition of thermotolerance on exposure to lethal heat shock temperature. The Cna-1RIP allele was dominant over the wild type cna-1 allele, suggesting that the CNA-1RIP mutant protein acts in a dominant-negative manner. In addition, we studied calcineurin regulatory subunit (cnb-1) mutants, which were previously generated using RIP. The cnb-1RIP mutants showed sensitivity to calcium (Ca2+) and heat-shock stress conditions. Thus, calcineurin plays an essential role for vegetative and sexual developments, and tolerance to stress conditions in N. crassa. Moreover, CNA-1 directly interacts with the calmodulin (CaM) and calcineurin-responsive zinc finger-1 (CRZ-1) proteins under high Ca2+ condition in N. crassa.

Heat‐stress Memory is Responsible for Acquired Thermotolerance in Bangia fuscopurpurea

The environmental stresses that sessile organisms experience usually fluctuate dramatically and are often recurrent. Terrestrial plants can acquire memory of exposure to sublethal heat stress to acquire thermotolerance and survive subsequent lethal high-temperature stress; however, little is known concerning whether seaweeds acquire thermotolerance via heat-stress memory. We have demonstrated that the red seaweed Bangia fuscopurpurea can indeed acquire memory of sublethal high-temperature stress, resulting in the acquisition of thermotolerance that protects against subsequent lethal high-temperature stress. Moreover, the maintenance of heat-stress memory was associated with a slight increase in the saturation level of membrane fatty acids. This suggests that the modification of membrane fluidity via changes in membrane fatty acid composition is involved in the establishment and maintenance of heat-stress memory in B.fuscopurpurea. These findings provide insights into the physiological survival and growth strategies of sessile red seaweeds to cope with recurrent changes in environmental conditions.

Involvement of Stat3 phosphorylation in mild heat shock-induced thermotolerance

Thermotolerance is a phenomenon in which cells become resistant to stress by prior exposure to heat shock, and its development is associated with the induction of heat shock proteins (Hsps), including Hsp70. We previously showed that the expression of Hsp70 is regulated by the cytokine signaling transcription factor Stat3, but the role of Stat3 in thermotolerance is not known. In this study, we examined the possible involvement of Stat3 in the acquisition of thermotolerance. We found that severe heat shock-induced morphological changes and decreases in cell viability, which were suppressed by exposure to non-lethal mild heat shock prior to severe heat shock. This thermotolerance development was accompanied by Stat3 phosphorylation and the induction of Hsps such as Hsp105, Hsp70, and Hsp27. Stat3 phosphorylation and Hsp induction were inhibited by AG490, an inhibitor of JAK tyrosine kinase. Consistent with this, we found that mild heat shock-induced thermotolerance was partially suppressed by AG490 or knockdown of Hsp105. We also found that the Stat3 inhibitor Stattic suppresses the acquisition of thermotolerance by inhibiting the mild heat shock-induced Stat3 phosphorylation and Hsp105 expression. These results suggest that the mild heat shock-dependent stimulation of the JAK-Stat signaling pathway contributes to the development of thermotolerance via the induction of Hsps including Hsp105. This signaling pathway may be a useful target for hyperthermia cancer therapy.

Effect of thermal manipulation of broilers embryos on the response to heat-induced oxidative stress.

Effects of embryonic thermal manipulation (TM) on mRNA expressional levels and total antioxidant capacity of genes associated with heat-induced oxidative stress (NOX4, GpX2, SOD2, catalase, and AvUCP) in 2 breeds of broiler chicken were investigated. Fertile Cobb and Hubbard eggs (n = 1,200) were divided into 4 treatment groups: Cobb control, Cobb TM, Hubbard control, and Hubbard TM. Control groups were maintained under standard conditions (37.8°C; 56% relative humidity), whereas TM groups were incubated at 39°C and 65% relative humidity for 18 h a day from embryonic days (ED) 10 to 18. On post-hatch day 28, the broilers were subject to acute heat stress (AHS) at 40°C for 7 h. At certain intervals (0, 1, 3, 5, and 7h), 12 chickens from each of the 4 groups were humanely euthanized, and liver samples were immediately isolated. During AHS, in both breeds, the mRNA expression levels of NOX4, GPx2, SOD2, and catalase in TM chickens were significantly lower than in controls, but AvUCP mRNA expression in the TM group was higher. The total antioxidant capacity and activity of superoxidase dismutase and catalase were significantly lower in the TM than in the control group in both breeds. The results of this study suggest that TM has a long-lasting effect on the acquisition of thermotolerance in 2 broiler chicken breeds as indicated by the reduction of system genes associated with heat-induced oxidative stress.

Light priming of thermotolerance development in plants

ABSTRACTIt is widely perceived that plant responses to environmental temperatures are profoundly influenced by light conditions. However, it is unknown how light signals modulate plant thermal responses and what photoreceptors are responsible for the light regulation of thermal adaptive process. We have recently reported that phytochrome B (phyB)-mediated red light signals prime the ASCORBATE PEROXIDASE 2 (APX2)-mediated detoxification reaction of reactive oxygen species (ROS), a well-known biochemical process that mediates the acquisition of thermotolerance under high temperature conditions. It is interesting that red light influences the HEAT SHOCK FACTOR A1 (HSFA1)-stimulated activation of the APX2 transcription, which is otherwise responsive primarily to stressful high temperatures. Blue light also efficiently primes the APX2-mediated induction of thermotolerance. In natural habitats, temperatures fluctuate according to the light/dark cycles with temperature peaks occurring during the daytime. It is thus apparent that plants utilize light information to prepare for upcoming high temperature spells.

Cellular and epigenetic changes induced by heat stress in bovine preimplantation embryos.

Exposure of the preimplantation embryo to heat stress triggers a series of cellular, molecular, and adaptive changes preventing a normal embryonic development. Heat stress disrupts the embryo cytoskeleton, intracellular calcium levels, mitochondrial function, and induces apoptosis. Moreover, heat stress can act indirectly through induction of reactive oxygen species (ROS), leading to a variety of cellular damage. Embryonic resistance to heat shock is determined by factors such as genotype, developmental stage, apoptosis, redox status, and regulatory molecules. The early embryo is very susceptible to heat stress; it acquires resistance to elevated temperature as development advances. One of the mechanisms involved in the developmental acquisition of thermotolerance is heat-induced apoptosis, which acts as a quality control mechanism to remove damaged blastomeres allowing the embryo to survive after stress. Although embryos at >8-cell stage can activate the apoptotic cascade as an adaptive response to stress, embryos at the two-cell stage are resistant to proapoptotic signals. This lack of apoptotic response has been associated to mitochondrial resistance to depolarization and epigenetic regulations, such as DNA methylation and histone deacetylation. Even though the cellular mechanisms triggered by heat stress have been studied, very little attention has been paid to the vulnerability of the epigenome to drastic temperature changes during the preimplantation period. Therefore, this review aims to characterize the effects of elevated temperature on the bovine embryo, especially addresissing developmental, cellular, and epigenetic alterations triggered in response to temperature.