Hsp60 protein pattern in coral is altered by environmental changes in light and temperature

The heat shock protein Hsp60 exhibited marked oscillation during a 12-hour day period when the coral Turbinaria reniformis was maintained in the laboratory under constant conditions of light (200 μE) and temperature (27 °C). A biphasic pattern of Hsp60 was apparent, punctuated by a low protein level at the midpoint of the 12-hour day period. Oscillation of Hsp60 was also apparent when coral was kept in darkness in lieu of a scheduled light period. The pattern of Hsp60 was altered when coral was exposed to increased light intensity (400 μE) or temperature elevation (32 °C). These observations suggest that Hsp60 in coral exhibits oscillation that is altered by increased light and temperature elevation.     

Water flow influences oxygen transport and photosynthetic efficiency in corals

Recent studies indicate that the incidence and persistence of damage from coral reef bleaching are often highest in areas of restricted water motion, and that resistance to and recovery from bleaching is increased by enhanced water motion. We examined the hypothesis that water motion increases the efflux of oxygen from coral tissue thereby reducing oxidative stress on the photosynthetic apparatus of endosymbiotic zooxanthellae. We experimentally exposed colonies of Montastrea annularis and Agaricia agaricites to manipulations of water flow, light intensity, and oxygen concentration in the field using a novel mini-flume. We measured photosynthetic efficiency using a pulse amplitude modulated fluorometer to test the short-term response of corals to our manipulations. Under normal oxygen concentrations, A. agaricites showed a significant 8% increase in photosynthetic efficiency from 0.238 (± 0.032) in still water to 0.256 (± 0.037) in 15 cm s⁻¹ flow, while M. annularis exhibited no detectable change. Under high-ambient oxygen concentrations, the observed effect of flow on A. agaricites was reversed: photosynthetic efficiencies showed a significant 11% decrease from 0.236 (± 0.056) in still water to 0.211 (± 0.048) in 15 cm s⁻¹ flow. These results support the hypothesis that water motion helps to remove oxygen from coral tissues during periods of maximal photosynthesis. Flow mitigation of oxidative stress may at least partially explain the increased incidence and severity of coral bleaching in low flow areas and observations of enhanced recovery in high-flow areas.     

Role of HSF activation for resistance to heat, cold and high-temperature knock-down

Regulation of heat shock proteins (Hsps) by the heat shock factor (HSF) and the importance of these proteins for resistance to heat stress is well documented. Less characterized is the importance of Hsps for cold stress resistance although Hsp70 is known to be induced following long-term cold exposure in Drosophila melanogaster. In this study, a temperature-sensitive HSF mutant line was used to investigate the role of HSF activation following heat hardening, rapid cold hardening (RCH) and long-term cold acclimation (LTCA) on heat and cold resistance, and this was correlated with Hsp70 expression. In addition, the effect of HSF activation on high-temperature knock-down resistance was evaluated. We found a significantly decreased HSF activation in the mutant line as compared to a corresponding control line following heat hardening, and this was correlated with decreased heat resistance of the mutant line. However, we did not find this difference in HSF activity to be important for resistance to cold stress or high-temperature knock-down. The findings indicate that induction of stress genes regulated by HSF, such as Hsps, although occurring following LTCA, are not of major importance for cold stress resistance and neither for RCH nor high-temperature knock-down resistance in D. melanogaster.     

Photosynthetic Thermotolerance is Quantitatively and Positively Correlated with Production of Specific Heat-shock Proteins Among Nine Genotypes of Lycopersicon (Tomato)

We recently showed that the chloroplast small heat-shock protein (herein referred to as chlp Hsp24) protects photosystem 2 (PS2) during heat stress, and phenotypic variation in production of chlp Hsp24 is positively related to PS2 thermotolerance. However, the importance of chlp Hsp24 or other Hsps to other aspects of photosynthesis and overall photosynthetic thermotolerance is unknown. To begin investigating this and the importance of genetic variation in Hsp production to photosynthetic thermotolerance, the production of several prominent Hsps and photosynthetic thermotolerance were quantified in nine genotypes of Lycopersicon, and then the relationships between thermotolerance of net photosynthetic rate (P _N) and production of each Hsp were examined. The nine genotypes exhibited wide variation in P _N thermotolerance and production of each of the Hsps examined (chlp Hsp70, Hsp60, and Hsp24, and cytosol Hsp70). No statistically significant relationship was observed between production of chlp Hsp70 and P _N thermotolerance, and only a weak positive relationship between cytosolic Hsp70 and P _N was detected. However, significant positive relationships were observed between production of chlp Hsp24 and Hsp60 and P _N thermotolerance. Hence natural variation in production of chlp Hsp24 and Hsp60 is important in determining variation in photosynthetic thermotolerance. This is perhaps the first evidence that chlp Hsp60 is involved in photosynthetic thermotolerance, and these in vivo results are consistent with previous in vitro results showing that chlp Hsp24 protects PS2 during heat stress.     

Cadmium and heat response of the fungus <Emphasis Type="Italic">Heliscus lugdunensis</Emphasis> isolated from highly polluted and unpolluted areas

Summary. Induction of heat shock protein (Hsp) 70 and distinct metallothionein-like proteins (MTLPs) in response to Cd and heat treatment were studied in two strains of the aquatic hyphomycete Heliscus lugdunensis: Hl-H4, isolated from a heavy metal polluted site, and Hl-BB taken from an unpolluted area. Upon Cd-exposure, Hsp70 was actively synthesized in the strain Hl-H4, and to a much lower degree in the strain Hl-BB. The Hsp70-expression was time- and dose-dependent, reaching a maximum after 24 h incubation with 80 μM Cd. Upon heat-stress, a similar response was observed: a strong Hsp70-expression in Hl-H4, and only a marginal one in Hl-BB. The strains reacted to Cd-exposure by a specific, environmentally related induction of MTLPs, as shown by the highly sensitive bimane derivatisation method of SH-rich proteins. In Hl-H4, a strong expression of 11 kDa MTLP was registered, which followed strictly the induction pattern of Hsp70. This suggests interdependence of the induction mechanisms and roles of these stress proteins in metal resistance. On the contrary, in Hl-BB a weak expression of MTLP of about 20 kDa was observed, exhibiting completely different induction pattern. The results suggest that the specific induction of Hsp70 and/or distinct MTLPs in the range of 11 kDa in H. lugdunensis strain Hl-H4 are essential adaptive mechanisms to continuous heavy metal exposure. Authors’ address: Assoc. Prof. Dr. Konstantin Grancharov, Bulgarian Academy of Sciences, Institute of Molecular Biology, Acad. G. Bonchev Str. Bl. 21, BG-1113 Sofia, Bulgaria     

Loss of Functional Photosystem II Reaction Centres in Zooxanthellae of Corals Exposed to Bleaching Conditions: Using Fluorescence Rise Kinetics

Mass coral bleaching is linked to elevated sea surface temperatures, 1-2 degrees C above average, during periods of intense light. These conditions induce the expulsion of zooxanthellae from the coral host in response to photosynthetic damage in the algal symbionts. The mechanism that triggers this release has not been clearly established and to further our knowledge of this process, fluorescence rise kinetics have been studied for the first time. Corals that were exposed to elevated temperature (33 degrees C) and light (280 mumol photons m(-2) s(-1)), showed distinct changes in the fast polyphasic induction of chlorophyll-a fluorescence, indicating biophysical changes in the photochemical processes. The fluorescence rise over the first 2000ms was monitored in three species of corals for up to 8 h, with a PEA fluorometer and an imaging-PAM. Pocillopora damicornis showed the least impact on photosynthetic apparatus, while Acropora nobilis was the most sensitive, with Cyphastrea serailia intermediate between the other two species. A. nobilis showed a remarkable capacity for recovery from bleaching conditions. For all three species, a steady decline in the slope of the initial rise and the height of the J-transient was observed, indicating the loss of functional Photosystem II (PS II) centres under elevated-temperature conditions. A significant loss of PS II centres was confirmed by a decline in photochemical quenching when exposed to bleaching stress. Non-photochemical quenching was identified as a significant mechanism for dissipating excess energy as heat under the bleaching conditions. Photophosphorylation could explain this decline in PS II activity. State transitions, a component of non-photochemical quenching, was a probable cause of the high non-photochemical quenching during bleaching and this mechanism is associated with the phosphorylation-induced dissociation of the light harvesting complexes from the PS II reaction centres. This reversible process may account for the coral recovery, particularly in A. nobilis.     

Expression and localization of Hsps in the heart and blood vessel of heat-stressed broilers

The objective of this study was to investigate the kinetics of Hsp60, Hsp70, Hsp90 protein, and messenger RNA (mRNA) expression levels and to correlate these heat shock protein (Hsp) levels with tissue damage resulting from exposure to high temperatures for varying amounts of time. One hundred broilers were heat-stressed for 0, 2, 3, 5, and 10 h, respectively, by rapidly increasing the ambient temperature from 22 +/- 1 degrees C to 37 +/- 1 degrees C. Obvious elevations of plasma creatine kinase indicate damage to myocardial cells after heat stress. Hsp70 and Hsp90, and their corresponding mRNAs in the heart tissue of heat-stressed broilers, elevated significantly after 2 h of heat exposure and decreased quickly with continued heat stress. However, the levels of hsp60 mRNA in the heart of heat-stressed broilers increased sharply (P < 0.01) at 2 h of heat stress but then decreased quickly after 3 h, while the level of Hsp60 protein in the heart increased (P < 0.01) at 2 h of heat stress and maintained a high level throughout heat exposure. The results indicate that the elevation of the three Hsps, especially Hsp60 in heart, may be important markers at the beginning of heat stress and act as protective proteins in adverse environments. The reduction of Hsp signals in the cytoplasm of myocardial cells implies that myocardial cell lesions may have an adverse impact on the function of Hsps during heat stress. Meanwhile, the localization of Hsp70 in blood vessels of broiler hearts suggests another possible mechanism for protection of the heart after heat exposure.     

Differential responses of stress proteins, antioxidant enzymes, and photosynthetic efficiency to physiological stresses in the Florida red tide dinoflagellate, Karenia brevis

This study identifies stress proteins and antioxidant enzymes that may play a role in the survival strategies of the Florida red tide dinoflagellate, Karenia brevis. Heat shock protein 60 (Hsp 60), mitochondrial small heat shock protein (mitosHsp), chloroplastic small heat shock protein (chlsHsp), Mn superoxide dismutase (SOD), and Fe SOD were first identified by Western blotting. The induction of these proteins in laboratory cultures in response to elevated temperatures, hydrogen peroxide, lead, or elevated light intensities was next assessed. In parallel, F(V)/F(M), a measurement of photosynthetic efficiency and common proxy of cellular stress, was determined. Hsp 60, Fe SOD, and Mn SOD were induced following exposure to elevated temperatures, hydrogen peroxide, or lead. MitosHsp responded only to heat, whereas chlsHsp responded only to H(2)O(2)-induced stress. The expression of stress proteins and antioxidant enzymes appears to be a more sensitive indicator of heat or chemically induced stresses than F(V)/F(M). However, F(V)/F(M) decreased significantly in response to elevated light intensities that did not induce the expression of stress proteins. These results identify for the first time stress proteins and antioxidant enzymes in K. brevis, provide evidence for differential sensitivity of cellular organelles to various sources of stress, and confirm the presence of conserved stress responses observed across phyla in a dinoflagellate.     

Effects of cold- and heat hardening on thermal resistance in Drosophila melanogaster

The effects of cold- and heat hardening on resistance to both low and high temperature stress was examined in Drosophila melanogaster lines selected for resistance to either cold or heat. The hardening effect was positive when the hardening was of the same type as the stress in all selection regimes. The effect of cold hardening on survival after heat stress was further examined in the lines selected for cold resistance and corresponding controls. A cross-protection effect (increased heat resistance after cold hardening) was present and this effect was lower in the lines selected for resistance to cold than in the controls. The level of Hsp70 expression induced by a non-lethal cold hardening was examined, showing that cold hardening induced Hsp70 expression. The results suggest that the cross-protection effect is at least partly due to Hsp70 expression induced by cold exposure.     

Cold stress induces antioxidants and Hsps in chicken immune organs

The aim of this study was to investigate the effects of cold stress on oxidative indexes, immune function, and the expression levels of heat shock protein (Hsp90, Hsp70, Hsp60, Hsp40, and Hsp27) in immune organs of chickens. Two hundred forty 15-day-old male chickens were randomly divided into 12 groups and kept under the temperature of (12 ± 1) °C for acute and chronic cold stress. There were one control group and five treatment groups for acute cold stress and three control groups and three treatment groups for chronic cold stress. The results showed that cold stress influence the activities of antioxidant enzymes in the immune organs. The activities of SOD and GSH-Px were first increased then decreased, and activity of total antioxidation capacity (T-AOC) was significantly decreased (P < 0.05) at the acute cold stress in chicks; however, T-AOC activities were significantly increased (P < 0.05) at the chronic cold stress in these tissues. Cold stress induced higher level of malondialdehyde (MDA) in chicken immune organs. In addition, the cytokine contents were increased in cold stress groups. As one protective factor, the expression levels of Hsps were increased significantly (P < 0.05) in both cold stress groups. These results suggested that cold stress induced the oxidative stress in the three tissues and influenced immune function of chicks. Higher expression of Hsps (Hsp90, Hsp70, Hsp60, Hsp40, and Hsp27) may play a role in protecting immune organs against cold stress.     

Water-restraint stress enhances methamphetamine-induced cardiotoxicity

Methamphetamine (MAP) and stress both cause a variety of cardiovascular problems. Stress also increases stimulant drug-seeking or drug-taking behavior by both humans and animals. In addition to the physiological effects on circulation, metabolism, and excretion, stress affects subject's responses to stimulant drugs such as MAP. However, the mechanisms underlying the drug–stress interactions remain unknown. In the present study, we assessed the effects of stress on myocardial responses to MAP in mice. Mice were injected with MAP (30 mg/kg) immediately before exposure to water-restraint stress (WRS), which has often been used as a stressor in animal experiments. The combination of MAP with WRS produced a significant increase (p < 0.01) in the leakage of proteins specific to myocardial damage and the levels of cytokines IL-6, TNF-α, and IL-10. The histological findings indicated the possibility that a combination of MAP with WRS induced cardiac myocytolysis. We also examined the expression of heat shock proteins (Hsps), which have cardioprotective effects. Administration of MAP alone significantly stimulated the RNA expressions of Hsp32, 60, 70, and 90 and the protein Hsp70 in cardiac muscles, whereas the expressions due to WRS or MAP plus WRS were not increased. These results reveal the fact that exposure to WRS depresses the induction of Hsps, in particular Hsp70, due to MAP injection, following to enhance MAP-induced myocardial damage. We believe that interactions between MAP and severe stress, including environmental temperature, affect the induction of Hsps, following to susceptibility of hosts to cardiotoxicity due to the stimulant drug.     

高山植物圆锥南芥的光合系统耐热性及其修复机制(英文)

高温胁迫包括极端高温和中高温,严重影响了植物的一系列生理活动,尤其是光合作用,而植物应对极端高温和中高温胁迫具有不同的策略。高山植物因长期生长于相对寒冷的环境中,相比而言应缺少对高温胁迫的适应机制。本文以圆锥南芥作为一种高山模式植物来探索其在中高温下是否表现出耐热能力,如果具有耐热能力,那么在光合方面与拟南芥存在怎样的差异。研究发现,圆锥南芥在中高温处理后具有更高的光化学效率及快速可逆的恢复过程,表现出了较强的耐热能力。两物种的F0没有明显的差异,而圆锥南芥在热处理后及恢复过程中具有更高的Fm,促进其快速光合修复。在热处理后,非光化学能量耗散快速瞬时上升,及时保护光系统II免受光损伤和热伤害,另外,HSP101蛋白迅速诱导可能启动了光化学修复。最后,圆锥南芥在严重高温处理后具有更高的存活率再次验证了它在中高温下的耐热能力。结果表明,圆锥南芥具有更耐热的光合系统以及有效的光合修复机制来耐受中高温胁迫。     

Expression of heat shock proteins in adult honey bee (Apis mellifera L.) workers under hot-arid subtropical ecosystems

Heat stress elicits the expression of heat shock proteins (HSPs) in honey bee subspecies. These highly conserved proteins have significant role in protecting cells from thermal-induced stresses. Honey bees in subtropical regions face extremely dry and hot environment. The expression of HSPs in the nurses and foragers of indigenous (Apis mellifera jemenitica) and imported European (Apis mellifera ligustica and Apis mellifera carnica) honey bee subspecies after heat shock treatment were compared using SDS-PAGE. Hsp70 and Hsp82 were equally expressed in the nurses of all tested bee subspecies when exposed to 40 °C and 45 °C for 4 h. The forager bees exhibited differential expression of HSPs after heat stress. No HSPs was expressed in the foragers of A. m. jemenitica, and Hsp70 was expressed only in the foragers of A. m. ligustica and A. m. carnica at 40 °C. A prominent diversity in HSPs expression was also exhibited in the foragers at 45 °C with one HSP (Hsp70) in A. m. jemenitica, two HSPs (Hsp40 and Hsp70) in A. m. carnica, and three HSPs (Hsp40, Hsp60 and Hsp70) in A. m. ligustica. No HSPs was expressed in the control nurse and forager bees at any of the tested temperatures. These findings illustrated the differences in HSP expression among nurse and forager bees. It is obvious that the native foragers are more heat tolerant with least HSPs expression than exotic bee races. Further investigations will help to understand the potential role of HSPs in the adaptability, survival, and performance of bee subspecies in harsh climate of the subtropical regions.     

Standardized short‐term acute heat stress assays resolve historical differences in coral thermotolerance across microhabitat reef sites

Coral bleaching is one of the main drivers of reef degradation. Most corals bleach and suffer mortality at just 1–2°C above their maximum monthly mean temperatures, but some species and genotypes resist or recover better than others. Here, we conducted a series of 18‐hr short‐term acute heat stress assays side‐by‐side with a 21‐day long‐term heat stress experiment to assess the ability of both approaches to resolve coral thermotolerance differences reflective of in situ reef temperature thresholds. Using a suite of physiological parameters (photosynthetic efficiency, coral whitening, chlorophyll a, host protein, algal symbiont counts, and algal type association), we assessed bleaching susceptibility of Stylophora pistillata colonies from the windward/exposed and leeward/protected sites of a nearshore coral reef in the central Red Sea, which had previously shown differential mortality during a natural bleaching event. Photosynthetic efficiency was most indicative of the expected higher thermal tolerance in corals from the protected reef site, denoted by an increased retention of dark‐adapted maximum quantum yields at higher temperatures. These differences were resolved using both experimental setups, as corroborated by a positive linear relationship, not observed for the other parameters. Notably, short‐term acute heat stress assays resolved per‐colony (genotype) differences that may have been masked by acclimation effects in the long‐term experiment. Using our newly developed portable experimental system termed the Coral Bleaching Automated Stress System (CBASS), we thus highlight the potential of mobile, standardized short‐term acute heat stress assays to resolve fine‐scale differences in coral thermotolerance. Accordingly, such a system may be suitable for large‐scale determination and complement existing approaches to identify resilient genotypes/reefs for downstream experimental examination and prioritization of reef sites for conservation/restoration. Development of such a framework is consistent with the recommendations of the National Academy of Sciences and the Reef Restoration and Adaptation Program committees for new intervention and restoration strategies.     

Effects of light, food availability and temperature stress on the function of photosystem II and photosystem I of coral symbionts

Background

Reef corals are heterotrophic coelenterates that achieve high productivity through their photosynthetic dinoflagellate symbionts. Excessive seawater temperature destabilises this symbiosis and causes corals to “bleach,” lowering their photosynthetic capacity. Bleaching poses a serious threat to the persistence of coral reefs on a global scale. Despite expanding research on the causes of bleaching, the mechanisms remain a subject of debate.

Methodology/Principal Findings

This study determined how light and food availability modulate the effects of temperature stress on photosynthesis in two reef coral species. We quantified the activities of Photosystem II, Photosystem I and whole chain electron transport under combinations of normal and stressful growth temperatures, moderate and high light levels and the presence or absence of feeding of the coral hosts. Our results show that PS1 function is comparatively robust against temperature stress in both species, whereas PS2 and whole chain electron transport are susceptible to temperature stress. In the symbiotic dinoflagellates of Stylophora pistillata the contents of chlorophyll and major photosynthetic complexes were primarily affected by food availability. In Turbinaria reniformis growth temperature was the dominant influence on the contents of the photosynthetic complexes. In both species feeding the host significantly protected photosynthetic function from high temperature stress.

Conclusions/Significance

Our findings support the photoinhibition model of coral bleaching and demonstrate that PS1 is not a major site for thermal damage during bleaching events. Feeding mitigates bleaching in two scleractinian corals, so that reef responses to temperature stresses will likely be influenced by the coinciding availabilities of prey for the host.     

Heat-Stress and Light-Stress Induce Different Cellular Pathologies in the Symbiotic Dinoflagellate during Coral Bleaching

Coral bleaching is a significant contributor to the worldwide degradation of coral reefs and is indicative of the termination of symbiosis between the coral host and its symbiotic algae (dinoflagellate; Symbiodinium sp. complex), usually by expulsion or xenophagy (symbiophagy) of its dinoflagellates. Herein, we provide evidence that during the earliest stages of environmentally induced bleaching, heat stress and light stress generate distinctly different pathomorphological changes in the chloroplasts, while a combined heat- and light-stress exposure induces both pathomorphologies; suggesting that these stressors act on the dinoflagellate by different mechanisms. Within the first 48 hours of a heat stress (32°C) under low-light conditions, heat stress induced decomposition of thylakoid structures before observation of extensive oxidative damage; thus it is the disorganization of the thylakoids that creates the conditions allowing photo-oxidative-stress. Conversely, during the first 48 hours of a light stress (2007 µmoles m⁻² s⁻¹ PAR) at 25°C, condensation or fusion of multiple thylakoid lamellae occurred coincidently with levels of oxidative damage products, implying that photo-oxidative stress causes the structural membrane damage within the chloroplasts. Exposure to combined heat- and light-stresses induced both pathomorphologies, confirming that these stressors acted on the dinoflagellate via different mechanisms. Within 72 hours of exposure to heat and/or light stresses, homeostatic processes (e.g., heat-shock protein and anti-oxidant enzyme response) were evident in the remaining intact dinoflagellates, regardless of the initiating stressor. Understanding the sequence of events during bleaching when triggered by different environmental stressors is important for predicting both severity and consequences of coral bleaching.     

Local Stressors Reduce Coral Resilience to Bleaching

Coral bleaching, during which corals lose their symbiotic dinoflagellates, typically corresponds with periods of intense heat stress, and appears to be increasing in frequency and geographic extent as the climate warms. A fundamental question in coral reef ecology is whether chronic local stress reduces coral resistance and resilience from episodic stress such as bleaching, or alternatively promotes acclimatization, potentially increasing resistance and resilience. Here we show that following a major bleaching event, Montastraea faveolata coral growth rates at sites with higher local anthropogenic stressors remained suppressed for at least 8 years, while coral growth rates at sites with lower stress recovered in 2–3 years. Instead of promoting acclimatization, our data indicate that background stress reduces coral fitness and resilience to episodic events. We also suggest that reducing chronic stress through local coral reef management efforts may increase coral resilience to global climate change.     

The past,present, and future of coral heat stress studies

The global loss and degradation of coral reefs, as a result of intensified frequency and severity of bleaching events, is a major concern. Evidence of heat stress affecting corals through loss of symbionts and consequent coral bleaching was first reported in the 1930s. However, it was not until the 1998 major global bleaching event that the urgency for heat stress studies became internationally recognized. Current efforts focus not only on examining the consequences of heat stress on corals but also on finding strategies to potentially improve thermal tolerance and aid coral reefs survival in future climate scenarios. Although initial studies were limited in comparison with modern technological tools, they provided the foundation for many of today's research methods and hypotheses. Technological advancements are providing new research prospects at a rapid pace. Understanding how coral heat stress studies have evolved is important for the critical assessment of their progress. This review summarizes the development of the field to date and assesses avenues for future research.     

Differential effect of oxidative stress on the apoptosis of early and late passage human diploid fibroblasts: implication of heat shock protein 60

Since an attenuated response to stress is a characteristic of senescence, a cellular senescence model was used to examine the mechanism of resistance against oxidative stress using human diploid fibroblasts (HDF). With increasing passage, the HDF showed increased production of reactive oxygen species (ROS). Late passage HDF were resistant to the lethal effects of oxidative stress, showing less cleavage of pro-caspase-3 and PARP than those of early ones. Since heat shock proteins (Hsps) are not only cytoprotective but also interfere with the apoptotic cascade, the expression patterns of Hsps during cellular senescence were next examined. Oxidative stress induced a decrease in the mitochondrial Hsp60 levels with a concomitant increase in the cytosolic Hsp60 levels in the early passage HDF, but not in late ones. To show that the resistance to oxidative stress is a specific effect of Hsp60, the levels of Hsp60 were knocked down by siRNA. As expected the Hsp60 knock-down cells were more resistant to oxidative stress. These findings show that Hsp60 is a key player in the resistance mechanism against oxidative stress and aging.     

Oxidative stress and seasonal coral bleaching

During the past two decades, coral reefs have experienced extensive degradation worldwide. One etiology for this global degradation is a syndrome known as coral bleaching. Mass coral bleaching events are correlated with increased sea-surface temperatures, however, the cellular mechanism underlying this phenomenon is uncertain. To determine if oxidative stress plays a mechanistic role in the process of sea-surface temperature-related coral bleaching, we examined corals along a depth transect in the Florida Keys over a single season that was characterized by unusually high sea-surface temperatures. We observed strong positive correlations between accumulation of oxidative damage products and bleaching in corals over a year of sampling. High levels of antioxidant enzymes and small heat-shock proteins were negatively correlated with levels of oxidative damage products. Corals that experienced oxidative stress had higher chaperonin levels and protein turnover activity. Our results indicate that coral bleaching is tightly coupled to the antioxidant and cellular stress capacity of the symbiotic coral, supporting the mechanistic model that coral bleaching (zooxanthellae loss) may be a final strategy to defend corals from oxidative stress.