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17 results for “Heat hardening”
Synchronization of seasonal acclimatization and short-term heat hardening improves physiological resilience in a changing climate
<p><b>Summary</b></p> <p>1. Animal survival and species distribution in the face of global warming and increasing occurrences of heatwave largely depend on how heat tolerance shifts with plastic responses at different spatiotemporal scales, including long-term acclimation/acclimatization and short-term heat hardening. However, knowledge about the interaction of these plastic responses is still unclear.</p> <p>2. To understand how plastic responses at different timescales work together to adjust heat tolerance of organisms, we examined the effect of heat hardening on the upper thermal limits of an intertidal mudflat bivalve, the razor clam <i>Sinonovacula constricta</i>, for different seasons by using heart rate as a proxy.</p> <p>3. We observed a stronger heat hardening response of<i> S. constricta</i> in warm seasons, implying that heat hardening worked synchronously with seasonal acclimatization to increase resistance of the clams to high temperatures in warm seasons. In warm seasons, heat hardening increased heat tolerance by 2-4<sup>°</sup>C and showed a 24-h temporal dependence, suggesting an adaptation to the diel fluctuation of thermal regimes in summer.</p> <p>4. Furthermore, thermal stress resembling seasonal maximum environmental temperature induced stronger heat hardening effects, indicating that heat hardening is an essential plastic response to extreme hot weather, complementing seasonal acclimatization.</p> <p>5. Our results suggest that high temperature risk can be alleviated jointly by seasonal acclimatization and heat hardening, and emphasize the importance of considering physiological plasticity on both long-term and short-term temporal scales in evaluating and forecasting vulnerability of organisms to climate change.</p>
Data from: Rapid heat hardening in embryos of the lizard Anolis sagrei
<p><span>Adaptive thermal tolerance plasticity can dampen the negative effects of warming. However, our knowledge of tolerance plasticity is lacking for embryonic stages that are relatively immobile and may benefit the most from an adaptive plastic response. We tested for heat hardening capacity (a rapid increase in thermal tolerance that manifests in minutes to hours) in embryos of the lizard <em>Anolis sagrei</em>. We compared survival of a lethal temperature exposure between embryos that either did ('hardened') or did not ('not hardened') receive a high but non-lethal temperature pre-treatment. We also measured heart rates at common garden temperatures before and after heat exposures to assess metabolic consequences. 'Hardened' embryos had significantly greater survival after lethal heat exposure relative to 'not hardened' embryos. That said, heat pre-treatment led to a subsequent increase in embryo heart rate that did not occur in embryos that did not receive pre-treatment, indicative of an energetic cost of mounting the heat hardening response. Our results are consistent with adaptive thermal tolerance plasticity in these embryos (greater heat survival after heat exposure), but also highlight associated costs. Thermal tolerance plasticity may be an important mechanism by which embryos respond to warming that warrants greater consideration. </span></p>
Synchronization of seasonal acclimatization and short-term heat hardening improves physiological resilience in a changing climate
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Data from: Rapid heat hardening in embryos of the lizard Anolis sagrei
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Hypoxia inducible factor-1α knockout does not impair acute thermal tolerance or heat hardening in zebrafish
The rapid increase in critical thermal maximum (CTmax) in fish (or other animals), previously exposed to critically high temperature is termed 'heat hardening', which likely represents a key strategy to cope with increasingly extreme environments. The physiological mechanisms that determine acute thermal tolerance, and the underlying pathways facilitating heat hardening, remain debated. It has been posited, however, that exposure to high temperature is associated with tissue hypoxia and may be associated with increased expression of hypoxia-inducible factor-1 (Hif-1). We studied acute thermal tolerance in zebrafish lacking functional Hif-1α paralogs (Hif-1aa and Hif-1ab double knockout; Hif-1α-/-), which are known to exhibit markedly reduced hypoxia tolerance. We hypothesised that Hif-1α-/- zebrafish would suffer reduced acute thermal tolerance relative to wild-types and that the heat hardening ability would be lost. On the contrary, we observed that Hif-1α-/- and wild-type fish did not differ in CTmax, and both genotypes exhibited heat hardening of a similar degree when CTmax was re-tested 48 h later. Despite exhibiting impaired hypoxia tolerance (based on loss of equilibrium experiments), Hif-1α-/- zebrafish display unaltered thermal tolerance, suggesting that these traits are not necessarily functionally associated. Hif-1α is accordingly not required for short-term acclimation in the form of heat hardening.
Data from: Rapid induction of the heat hardening response in an Arctic insect
<p><a name="_Hlk16601098">The ability to cope with increasing and more variable temperatures, due to predicted climate changes, through plastic and/or evolutionary responses will be crucial for the persistence of Arctic species. </a>Here, we investigate plasticity of heat tolerance of the Greenlandic seed bug <i>Nysius groenlandicus, </i>which inhabits areas with widely fluctuating temperatures. We test the heat resistance and hardening capacity (plasticity) of <i>N. groenlandicus </i>using both static (heat knock down time, HKDT) and dynamic (critical thermal maximum, CT<sub>max</sub>) assays. We find that <i>N. groenlandicus </i>is able to tolerate short-term exposure to temperatures up to almost 50°C and that it can quickly increase heat resistance following heat hardening. Further, we find that this hardening response is reversible within hours after hardening. These findings contrast with common observations from temperate and tropical insects and suggest that more attention should be given to species in extreme and thermally variable environments such as Arctic and subarctic regions.</p>
Data from: Does increased heat resistance result in higher susceptibility to predation? A test using (Drosophila melanogaster) selection and hardening
Heat resistance of ectotherms can be increased both by plasticity and evolution, but these effects may have trade-offs resulting from biotic interactions. Here we test for predation costs in <i>Drosophila melanogaster</i> populations with altered heat resistance produced by adult hardening and directional selection for increased heat resistance. In addition, we also tested for genetic trade-offs by testing heat resistance in lines that have evolved under increased predation risk. We show that while 35/37°C hardening increases heat resistance as expected, it does not increase predation risk from jumping spiders or mantids; in fact there was an indication that survival may have increased under predation following a triple 37°C compared to a single 35°C hardening treatment. Flies that survived a 39°C selection cycle showed lower survival under predation, suggesting a predation cost of exposure to a more severe heat stress. There was however no correlated response to selection because survival did not differ between control and selected lines after selection was relaxed for one or two generations. In addition, lines selected for increased predation risk did not differ in heat resistance. Our findings suggest independent evolutionary responses to predation and heat as measured in laboratory assays, and no costs of heat hardening on susceptibility to predation.
Membrane lipid metabolism, heat shock response, and energy costs mediate the interaction between acclimatization and heat hardening response
<p>Thermal plasticity on different timescales, including acclimation/acclimatization and heat hardening response – a rapid adjustment for thermal tolerance after a nonlethal thermal stress, can interact on organisms to improve the resilience to thermal stress. However, little is known about the physiological mechanisms mediating this interaction. To investigate underpinnings of heat hardening responses after acclimatization in warm season, we measured thermal tolerance plasticity, compared transcriptomic and metabolomic changes after heat hardening at 33 or 37<sup>o</sup>C followed by recovery of 3 h or 24 h in an intertidal bivalve <i>Sinonovacula constricta</i>. The clams showed explicit heat hardening responses after acclimatization in warm season. The higher inducing temperature (37<sup>o</sup>C) caused a less effective heat hardening effect than the inducing temperature that was closer to seasonal maximum temperature (33<sup>o</sup>C). Metabolomic analysis highlighted the elevated contents of membrane glyceropholipids in all heat hardened clams, which may help to maintain structure and function of membrane. Heat shock proteins (HSPs) tended to be up-regulated after heat hardening at 37<sup>o</sup>C but not at 33<sup>o</sup>C, indicating that there was no complete dependency of heat hardening effects on up-regulated HSPs. Enhanced energy metabolism and decreased energy reserves were observed after heat hardening at 37<sup>o</sup>C, suggesting more energy costs during exposure to higher inducing temperature which may restrict heat hardening effects. These results highlighted the mediating role of membrane lipid metabolism, heat shock responses and energy costs in the interaction of heat hardening response and seasonal acclimatization, and benefit the mechanistic understanding of evolutionary change and thermal plasticity during global climate change.</p>
Hypoxia inducible factor-1α knockout does not impair acute thermal tolerance or heat hardening in zebrafish
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Membrane lipid metabolism, heat shock response, and energy costs mediate the interaction between acclimatization and heat hardening response
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Data from: Does increased heat resistance result in higher susceptibility to predation? A test using (Drosophila melanogaster) selection and hardening
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Data from: Rapid induction of the heat hardening response in an Arctic insect
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Data from: Heat hardening capacity in Drosophila melanogaster is life stage specific and juveniles show the highest plasticity
Variations in stress resistance and adaptive plastic responses during ontogeny have rarely been addressed, despite the possibility that differences between life stages can affect species' range margins and thermal tolerance. Here, we assessed the thermal sensitivity and hardening capacity of Drosophila melanogaster across developmental stages from larval to the adult stage. We observed strong differences between life stages in heat resistance, with adults being most heat resistant followed by puparia, pupae and larvae. The impact of heat hardening (1 h at 35°C) on heat resistance changed during ontogeny, with the highest positive effect of hardening observed in puparia and pupae and the lowest in adults. These results suggest that immobile life stages (puparia and pupae) have evolved high plasticity in upper thermal limits whereas adults and larvae rely more on behavioural responses to heat stress allowing them to escape from extreme high temperatures. While most studies on the plasticity of heat resistance in ectotherms have focused on the adult life stage, our findings emphasize the crucial importance of juvenile life stages of arthropods in understanding the thermal biology and life stage-specific physiological responses to variable and stressful high temperatures. Failure to acknowledge this complication might lead to biased estimates of species' ability to cope with environmental changes, such as climate change.
Effects of heat hardening on life parameters and thermostability of Bradysia odoriphaga larva and adults
High temperature in summer is a key barrier for <i>Bradysia odoriphaga</i> (Diptera: Sciaridae), a serious pest of vegetables in China. Because mild heat hardening can enhance the thermotolerance of many insects, we determined if heat hardening was beneficial for <i>B. odoriphaga</i> adaptation to high summer temperatures. We studied the biological performance, antioxidant responses and <i>hsp70</i> and <i>hsp90</i> expression of <i>B. odoriphaga </i>4<sup>th</sup> instar larvae and adults after pre-exposure to mild heat hardening temperatures (30-36°C). The tolerance of larvae to severe heat stress was enhanced after mild heat hardening (32-36°C). However, life parameters were significantly inhibited, development was delayed, longevity was shortened and fecundity was decreased. Mild heat hardening (30-34°C) caused serious adverse effects on life parameters and less enhancement of heat resistance for 4<sup>th</sup> larvae. Mild heat hardening at 36°C weakened the heat tolerance of adults. The activity of four antioxidant enzymes in <i>B. odoriphaga</i> changed dramatically after heat hardening at 32-36°C. CAT and GST maintained successive higher activities, and POD also had higher activities in larvae after 48 h recovery at 25°C, pupae, and adults. Simultaneously, the expression levels<i> </i>of<i> hsp70</i> and <i>hsp90</i> increased significantly upon thermal hardening. Higher expression levels were also detected in larvae after 48 h recovery at 25°C, pupae, and adults. Mild heat hardening played an important role in heat tolerance plasticity of <i>B. odoriphaga</i> larvae. The antioxidant system and <i>hsp70</i> and <i>hsp90</i> genes were relevant to this adaptation process.
Heat hardening improves thermal tolerance in abalone, without the trade-offs associated with exposure to chronic elevated temperature
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Data from: Heat hardening capacity in Drosophila melanogaster is life stage specific and juveniles show the highest plasticity
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Effects of heat hardening on life parameters and thermostability of Bradysia odoriphaga larva and adults
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