Molecular genetics of heat tolerance and heat shock proteins in cereals

Heat stress is common in most cereal-growing areas of the world. In this paper, we summarize the current knowledge on the molecular and genetic basis of thermotolerance in vegetative and reproductive tissues of cereals. Significance of heat stress response and expression of heat shock proteins (HSPs) in thermotolerance of cereal yield and quality is discussed. Major avenues for increasing thermotolerance in cereals via conventional breeding or genetic modification are outlined.     

Elevation of the heat resistance of Salmonella typhimurium by sublethal heat shock

The survival of Salmonella typhimurium after a standard heat challenge at 55°C for 25 min increased by several orders of magnitude when cells grown at 37°C were pre-incubated at 42°, 45° or 48°C before heating at the higher temperature. Heat resistance increased rapidly after the temperature shift, reaching near maximum levels within 30 min. Elevated heat resistance persisted for at least 10 h. Preincubation of cells at 48°C for 30 min increased their resistance to subsequent heating at 50°, 52°, 55°, 57° or 59°C. Survival curves of resistant cells were curvilinear. Estimated times for a '7D' inactivation increased by 2.6- to 20-fold compared with cells not pre-incubated before heat challenge.     

Elevation of the heat resistance of Salmonella typhimurium by sublethal heat shock

The survival of Salmonella typhimurium after a standard heat challenge at 55 degrees C for 25 min increased by several orders of magnitude when cells grown at 37 degrees C were pre-incubated at 42 degrees, 45 degrees or 48 degrees C before heating at the higher temperature. Heat resistance increased rapidly after the temperature shift, reaching near maximum levels within 30 min. Elevated heat resistance persisted for at least 10 h. Pre-incubation of cells at 48 degrees C for 30 min increased their resistance to subsequent heating at 50 degrees, 52 degrees, 55 degrees, 57 degrees or 59 degrees C. Survival curves of resistant cells were curvilinear. Estimated times for a '7D' inactivation increased by 2.6- to 20-fold compared with cells not pre-incubated before heat challenge.     

Birgean heat budgets and rates of heat uptake in two monomictic lakes

Thermal profile development, rates of heat uptake and annual heat budgets are presented for two monomictic lakes, Whatcom and Washington, in the Puget Sound lowlands of Washington State. The rates of heat gain in the lakes were found to be significantly affected by lake morphometry. In turn, the differing rates of heat gain affected the annual heat budgets.     

Effect of prior heat shock on heat resistance of Listeria monocytogenes in meat

The effect of prior heat shock on the thermal resistance of Listeria monocytogenes in meat was investigated. A sausage mix inoculated with approximately 10(7) L. monocytogenes per g was initially subjected to a heat shock temperature of 48 degrees C before being heated at a final test temperature of 62 or 64 degrees C. Although cells heat shocked at 48 degrees C for 30 or 60 min did not show a significant increase in thermotolerance as compared with control cells (non-heat shocked), bacteria heat shocked for 120 min did, showing an average 2.4-fold increase in the D64 degrees C value. Heat-shocked cells shifted to 4 degrees C appeared to maintain their thermotolerance for at least 24 h after heat shock.     

Adaptation to heat of cardiomyoblasts in culture protects them against heat shock: role of nitric oxide and heat shock proteins

Dosed adaptation to environmental factors is an efficient non-drug means for increasing the resistance of organs or the body as a whole. We demonstrated earlier that nitric oxide (NO) plays an important role in adaptive defense of the organism, in particular due to activation of heat shock protein (HSP) synthesis. A key question remained open—to what extent the formation of adaptive defense depends on central mechanisms and to what extent on the intracellular mechanisms immediately responding to the adapting factor, and whether the NO-dependent activation of HSP synthesis plays a role in adaptation of isolated cells. In the present study we looked into the possibility of producing a protective effect of adaptation to heat in cell culture. A 6-day adaptation to heat limited to 17% the decrease in metabolic activity induced by heat shock in H9c2 cardiomyoblasts. The development of adaptation was associated with increased NO production. Treatment of cells with the inhibitor of NO synthase L-NNA (100 M) prevented the development of adaptive protection. Adaptation of cell culture enhanced synthesis of HSP70 but not HSP27. Blockade of HSP70 synthesis with quercetin (50 M) left unchanged the protective effect of adaptation. Inhibition of NO synthesis restricted the adaptation-induced HSP70 synthesis. Therefore, the formation of adaptation at the cell level may result from a direct action of an environmental factor without participation of neurohumoral factors. Such adaptation involves NO-dependent mechanisms divorced from the activation of HSP70 synthesis.     

Convective heat transfer measured directly with a heat flux sensor

A heat flux disk has been developed that directly measures the convective heat transfer in W/m2. When the sensor is calibrated on an aluminum cylinder, the calibration constant obtained is greatest in still air. As air movement increases, the calibration constant is reduced with increasing convective heat transfer coefficient, 0.5%.W-1.m2.K. The influence of wind on the calibration value is greatly reduced when the sensor is attached to a surface with lower thermal conductivity. The local convective heat transfer coefficient (hc) of the human body was measured. The leg acts in a manner similar to that of a cylinder, with the highest hc value at the front facing the wind and the lowest approximately 90 degrees from the wind, and in the wake a value is obtained that is close to the average hc value of the leg. When hc is measured at several angles and positions all over the body, the results indicate that the body acts approximately as a cylinder with a hc value related to the wind speed as hc = 8.6.v0.6 W.m-2.K-1, where v is velocity.     

CHIP interacts with heat shock factor 1 during heat stress

Heat shock factor 1 (HSF1) is a major transactivator of heat shock genes in response to stress and mediates cell protection against various harmful conditions. In this study, we identified the interaction of CHIP (carboxyl terminus of the heat shock cognate protein 70-interacting protein) with the N-terminus of HSF1. Using GST full-down assay, we found that CHIP directly interacts with C-terminal deleted HSF1 (a.a. 1-290) but not with full-length HSF1 under non-stressed conditions. Interestingly, interaction of CHIP with full-length HSF1 was induced by heat shock treatment. The structural change of HSF1 was observed under heat stressed conditions by CD spectra. These observations demonstrate the direct interaction between HSF1 and CHIP and this interaction requires conformational change of HSF1 by heat stress.     

Isoproterenol sensitivity in heat tolerant and relatively heat intolerant men

Recent research has demonstrated that pharmacologic blockade of beta-adrenoceptors predisposes to hyperthermia during prolonged exercise. To investigate the hypothesis that beta-adrenoceptor sensitivity to catecholamines may be an important determinant of exertional heat tolerance, we performed a cross-sectional study comparing the heart rate responses to graded doses of isoproterenol in 6 heat tolerant and 6 relatively heat intolerant men. We observed no significant difference (p greater than 0.1) between the heat tolerant (0.9 +/- 0.68 microgram) and heat intolerant (1.19 +/- 0.61 microgram) subjects in the dose of isoproterenol that produced a 25 beat.min-1 increment in heart rate. Although the possibility of a relationship between beta-adrenoceptor sensitivity and the ability to tolerate exercise in heat cannot be entirely excluded on the basis of these data, our study clearly demonstrates the lack of a correlation between cardiac pacemaker sensitivity to isoproterenol and exertional heat tolerance.     

Extreme heat changes post‐heat wave community reassembly

Climate forecasts project further increases in extremely high‐temperature events. These present threats to biodiversity, as they promote population declines and local species extinctions. This implies that ecological communities will need to rely more strongly on recovery processes, such as recolonization from a meta‐community context. It is poorly understood how differences in extreme event intensity change the outcome of subsequent community reassembly and if such extremes modify the biotic environment in ways that would prevent the successful re‐establishment of lost species. We studied replicated aquatic communities consisting of algae and herbivorous rotifers in a design that involved a control and two different heat wave intensity treatments (29°C and 39°C). Animal species that suffered heat‐induced extinction were subsequently re‐introduced at the same time and density, in each of the two treatments. The 39°C treatment led to community closure in all replicates, meaning that a previously successful herbivore species could not re‐establish itself in the postheat wave community. In contrast, such closure never occurred after a 29°C event. Heat wave intensity determined the number of herbivore extinctions and strongly affected algal relative abundances. Re‐introduced herbivore species were thus confronted with significantly different food environments. This ecological legacy generated by heat wave intensity led to differences in the failure or success of herbivore species re‐introductions. Reassembly was significantly more variable, and hence less predictable, after an extreme heat wave, and was more canalized after a moderate one. Our results pertain to relatively simple communities, but they suggest that ecological legacies introduced by extremely high‐temperature events may change subsequent ecological recovery and even prevent the successful re‐establishment of lost species. Knowing the processes promoting and preventing ecological recovery is crucial to the success of species re‐introduction programs and to our ability to restore ecosystems damaged by environmental extremes.     

Interaction of the Neurospora crassa heat shock factor with the heat shock element during heat shock and different developmental stages

The interaction of the heat shock factor (HSF) with the heat shock element (HSE) was determined by a non-radioactive electrophoretic mobility shift assay, in order to analyze HSF regulation in Neurospora crassa. HSF binds to HSE under normal, non-stress conditions and is thus constitutively trimerized. Upon heat shock, the HSF-HSE complex shows a retarded mobility. This was also observed in Saccharomyces cerevisiae, where this mobility shift was shown to be due to HSF phosphorylation [Sorger and Pelham (1988) Cell 54, 855-864]. In N. crassa, HSE-dependent electrophoretic mobility shift is temperature- and time-dependent. Under normal growth conditions, the HSF is located in the cytoplasm as well as in the nucleus. In germinating conidia the HSF shows a retarded mobility typical for heat shock even at normal growth temperatures. No HSF-dependent mobility shift was detectable in aerial hyphae.     

Effects of heat shock,heat exposure pattern,and heat hardening on survival of the sycamore lace bug,Corythucha ciliata

The sycamore lace bug, Corythucha ciliata (Say) (Hemiptera: Tingidae), is an invasive exotic pest on Platanus trees in China. This study assessed the thermotolerance of C. ciliata in the laboratory. Detailed experiments were conducted on the effects of high temperature (35, 37, 39, 41, 43, and 45 °C), duration of exposure (0.5, 1, 2, 4, 6, and 8 h), and developmental stage (egg, nymph, and adult) on survival of the bug. Meanwhile, the effects of heat hardening on survival at lethal temperature (exposure to 33, 35, 37, 39, and 41 °C for 1 h prior to transfer to 43 °C for 2 h) were also assessed for nymphs and adults. Survival of eggs, nymphs, and adults was not affected by temperatures between 35 and 39 °C, but declined rapidly with increasing duration of exposure (from 0.5 to 8 h) at temperatures ≥41 °C. The lethal temperature that caused mortality of 50% (Ltemp₅₀) of all developmental stages decreased with increasing duration of exposure from 0.5 to 8 h. The Ltemp₅₀ for nymphs was 44.3, 42.0, and 39.0 °C after 0.5, 2, and 8 h exposure, respectively. Thermotolerance was the highest in eggs, followed by adults and then nymphs. Thermotolerance was slightly greater for adult males than for adult females. The ability of nymphs, females, and males to survive exposure to 43 °C for 2 h significantly increased by heat hardening, i.e., by exposure to a non‐lethal high temperature for 1 h; the optimal heat‐hardening temperature was 37 °C. The results indicate that survival of C. ciliata at heat‐shock temperatures depended on both the temperature and the duration of exposure, and the tolerance to heat shock was enhanced by heat hardening. The thermotolerance of C. ciliata may partially explain why C. ciliata has been rapidly spreading on Platanus trees in southern provinces of China.