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PubMed2002

Interspecific- and acclimation-induced variation in levels of heat-shock proteins 70 (hsp70) and 90 (hsp90) and heat-shock transcription factor-1 (HSF1) in congeneric marine snails (genus Tegula): implications for regulation of hsp gene expression.

In our previous studies of heat-shock protein (hsp) expression in congeneric marine gastropods of the genus Tegula, we observed interspecific and acclimation-induced variation in the temperatures at which heat-shock gene expression is induced (T(on)). To investigate the factors responsible for these inter- and intraspecific differences in T(on), we tested the predictions of the 'cellular thermometer' model for the transcriptional regulation of hsp expression. According to this model, hsps not active in chaperoning unfolded proteins bind to a transcription factor, heat-shock factor-1 (HSF1), thereby reducing the levels of free HSF1 that are available to bind to the heat-shock element, a regulatory element upstream of hsp genes. Under stress, hsps bind to denatured proteins, releasing HSF1, which can now activate hsp gene transcription. Thus, elevated levels of heat-shock proteins of the 40, 70 and 90 kDa families (hsp 40, hsp70 and hsp90, respectively) would be predicted to elevate T(on). Conversely, elevated levels of HSF1 would be predicted to decrease T(on). Following laboratory acclimation to 13, 18 and 23 degrees C, we used solid-phase immunochemistry (western analysis) to quantify endogenous levels of two hsp70 isoforms (hsp74 and hsp72), hsp90 and HSF1 in the low- to mid-intertidal species Tegula funebralis and in two subtidal to low-intertidal congeners, T. brunnea and T. montereyi. We found higher endogenous levels of hsp72 (a strongly heat-induced isoform) at 13 and 18 degrees C in T. funebralis in comparison with T. brunnea and T. montereyi. However, T. funebralis also had higher levels of HSF1 than its congeners. The higher levels of HSF1 in T. funebralis cannot, within the framework of the cellular thermometer model, account for the higher T(on) observed for this species, although they may explain why T. funebralis is able to induce the heat-shock response more rapidly than T. brunnea. However, the cellular thermometer model does appear to explain the cause of the increases in T(on) that occurred during warm acclimation of the two subtidal species, in which warm acclimation was accompanied by increased levels of hsp72, hsp74 and hsp90, whereas levels of HSF1 remained stable. T. funebralis, which experiences greater heat stress than its subtidal congeners, consistently had higher ratios of hsp72 to hsp74 than its congeners, although the sum of levels of the two isoforms was similar for all three species except at the highest acclimation temperature (23 degrees C). The ratio of hsp72 to hsp74 may provide a more accurate estimate of environmental heat stress than the total concentrations of both hsp70 isoforms.

Acclimatization↗
PubMed1989

Heat protectors and heat-induced preferential redistribution of 26 and 70 kDa proteins in Chinese hamster ovary cells.

An overall increase of 40% in nuclear-associated protein has been shown to be one of the sequellae of exposure of eukaryotic cells to elevated temperatures. Several investigators have shown that the increased protein/DNA ratios correlated well with the degree of cytotoxicity. In previous investigations, we have shown that cycloheximide, which protects the cell from the killing effects of heat, produces a dramatic reduction of the bulk nuclear-associated proteins after heating. In this investigation, we studied a previously unobserved efflux of a 26 kDa protein after heat shock and the preferential accumulation of the 70 kDa protein. The 26 kDa protein was shown not to be a member of previously described heat shock protein families. Preferential reduction of a 26 kDa protein and accumulation of a 70 kDa protein was observed in nuclei isolated from Chinese hamster ovary cells after heating at 43 degrees C. After heat treatment, the 26 kDa protein in the nucleus was decreased to a level 0.1-0.3 times the original amount in unheated cells, and the 70 kDa protein in the nucleus increased by a factor of 1.6-1.8. The normal levels of these two proteins were restored when cells were incubated at 37 degrees C following heat shock. Cells treated with heat protectors, cycloheximide and histidinol, demonstrated approximately the same redistribution in nuclear 26 and 70 kDa proteins immediately after heating as those not exposed to these drugs. On the other hand, restoration to control levels was much faster in the protector-treated cells, suggesting that "repair" of heat-induced damage is an important factor in the cells ability to survive this insult. Return to normal protein levels did not require new protein synthesis.

Animals↗
PubMed1983

Body heat balance in man subjected to endogenous and exogenous heat load.

The body heat balance, measured by a thermometric method, was investigated in humans subjected to endogenous and exogenous heat load. The purpose of the present study was to test the concept of heat exchange by a servomechanism in human thermoregulation. Two series of experiments were performed on male volunteers. In series I 15 subjects performed physical exercise (50% VO2 max) for 60 min at a constant ambient temperature of 25 degrees C. In series II 16 subjects rested in a climatic chamber where the ambient temperature was elevated over 30 min from 22 to 42 degrees C and kept stable at this level during the subsequent 60 min. It was found that in both series of experiments the sweating rate followed an exponential curve exhibiting an inertial course. Heat was stored in the body mainly at the beginning of experiment. In series I the net body heat load of 125 W/m2 was equalized by sweat evaporation, beginning after 40 min of the exercise. In series II the net body heat load of 80 W/m2 was equalized in the same way, starting after 35 min of the constant high ambient temperature. In both series of experiments the amount of heat stored in the body calculated from the body heat balance was quite close to the amount of heat calculated from the calorimetric equation. It is concluded, that under the present experimental conditions, heat loss from the body by sweat evaporation seems to be a regulated variable in the human thermoregulatory system. The observed increase in rectal temperature may result from an inertial course of the sweating reaction.

Adult↗
PubMed1984

A study of the effects of prior heat treatment on the skin reaction of mouse feet after heat alone or combined with X-rays: influence of misonidazole.

The skin of mouse feet was used to study the effects of hyperthermic treatment, either alone or combined with irradiation. The present experiments show that a priming heat treatment induces resistance both to a subsequent heat treatment and to a subsequent combined irradiation-heat treatment. The development of resistance to a combined irradiation-heat treatment after a priming heat treatment (30 min at 43 degrees C) was relatively slow (18-24 h) compared to development of resistance to a heat treatment without irradiation (6 h). Misonidazole, when administered prior to heat treatment only, did not influence the heat-induced skin reaction. However, when misonidazole was administered prior to combined irradiation-heat treatment, a slight but significant increase of the skin reaction was observed. Also, in combination with misonidazole resistance to combined treatment was observed by a priming heat treatment.

Animals↗
PubMed2003

Effect of resiniferatoxin on the noxious heat threshold temperature in the rat: a novel heat allodynia model sensitive to analgesics.

1. An increasing-temperature hot plate (ITHP) was introduced to measure the noxious heat threshold (45.3+/-0.3 degrees C) of unrestrained rats, which was reproducible upon repeated determinations at intervals of 5 or 30 min or 1 day. 2. Morphine, diclofenac and paracetamol caused an elevation of the noxious heat threshold following i.p. pretreatment, the minimum effective doses being 3, 10 and 200 mg kg(-1), respectively. 3. Unilateral intraplantar injection of the VR1 receptor agonist resiniferatoxin (RTX, 0.048 nmol) induced a profound drop of heat threshold to the innocuous range with a maximal effect (8-10 degrees C drop) 5 min after RTX administration. This heat allodynia was inhibited by pretreatment with morphine, diclofenac and paracetamol, the minimum effective doses being 1, 1 and 100 mg kg(-1) i.p., respectively. 4. The long-term sensory desensitizing effect of RTX was examined by bilateral intraplantar injection (0.048 nmol per paw) which produced, after an initial threshold drop, an elevation (up to 2.9+/-0.5 degrees C) of heat threshold lasting for 5 days. 5. The VR1 receptor antagonist iodo-resiniferatoxin (I-RTX, 0.05 nmol intraplantarly) inhibited by 51% the heat threshold-lowering effect of intraplantar RTX but not alpha,beta-methylene-ATP (0.3 micromol per paw). I-RTX (0.1 or 1 nmol per paw) failed to alter the heat threshold either acutely (5-60 min) or on the long-term (5 days). The heat threshold of VR1 receptor knockout mice was not different from that of wild-type animals (45.6+/-0.5 vs 45.2+/-0.4 degrees C). 6. In conclusion, the RTX-induced drop of heat threshold measured by the ITHP is a novel heat allodynia model exhibiting a high sensitivity to analgesics.

Acetaminophen↗
PubMed1991

[Heat radiation--an essential factor of heat transport in caloric vestibular tests? Current experimental findings].

According to the accepted theory, in vestibular testing the caloric stimulus is transported from the auditory canal to the lateral semicircular canal by heat conduction via the bone. Some findings, however, are not consistent with this concept, e.g. the short latency of the vestibular response, and the fact that removing of the osseous bridge does not stop the transport of heat to the semicircular canal. Physically there are three modes of heat transport: conduction, convection, and radiation. So far, only the first two have been discussed with regard to vestibular calorization, however, they fail to explain the findings mentioned above. We carried out experiments on 10 cadaveric temporal bone specimens in order to evaluate the possible effect of heat radiation. With experimental conditions strictly regulated (specimens kept in climate box, 37 degrees C, saturated humidity, standardized irrigation of the auditory canal with 50 ml of water of 50 degrees C in 15 sec., temperature measured by thermistors at selected points of the specimen), the deviation in repeated experiments was within 0.1 degree C. In normal temporal bones a spreading of heat along the osseous structures was found in accordance with heat conduction via the bone. Then the bony bridge between posterior frame of the tympanic membrane and the lateral canal was removed along with the tegmen tympani, leaving the auditory canal and labyrinth connected only by a small anterior-inferior strut. The rise of temperature in the lateral canal, however, was not delayed and reduced, as expected, but faster and greater than in the original situation. If, now, a reflecting shield was inserted in the cleft between tympanic membrane and labyrinth the heat transfer was dramatically reduced. A similar effect could be achieved in the intact middle ear by a shield or by filling the cavity with gel. Convection as means of heat transport could be excluded. The experiments show that heat transport in the vestibular calorization is a complex process, which besides heat conduction involves radiation as an essential factor. This explains a number of experimental and clinical findings that, so far, had been unclear.

Bone Conduction↗
PubMed2005

Secondary heat hyperalgesia detected by radiant heat stimuli in humans: evaluation of stimulus intensity and duration.

Diverging observations on secondary hyperalgesia to heat stimuli have been reported in the literature. No studies have investigated the importance of heat stimulus intensity and duration for the assessment of secondary heat hyperalgesia. The present study was designed to investigate systematically (1) if pain sensitivity to radiant heat stimuli (focused Xenon light) is altered in the area of secondary punctuate hyperalgesia induced by intradermal injection of capsaicin and (2) if heat stimulus duration and intensity had an influence on the ability to detect secondary heat hyperalgesia. Pain ratings to radiant heat stimuli from a focused xenon lamp were assessed within the area of secondary punctuate hyperalgesia in fifteen volunteers before and after intradermal injection of capsaicin. The stimulus conditions were systematically varied between three intensity levels (0.8, 1.0 and 1.2 x heat pain threshold (PT)) and four duration steps (200, 350, 500 and 750 ms). The present study shows that long duration (350-750 ms) and low intensity (0.8 and 1.0 x PT) radiant heat stimuli were adequate to detect secondary heat hyperalgesia.

Adult↗
PubMed1990

Heat shock proteins are not required for the degradation of alpha-amylase mRNA and the delamellation of endoplasmic reticulum in heat-stressed barley aleurone cells.

When barley (Hordeum vulgare) aleurone layers are heat shocked, the synthesis and secretion of alpha-amylase and other secretory proteins is arrested and the synthesis of heat shock proteins (hsps) is induced. alpha-Amylase mRNA, normally a very stable mRNA, is actively degraded during heat shock. In addition, endoplasmic reticulum (ER) is delamellated during heat shock, possibly causing the destabilization of the mRNA for the secreted alpha-amylase. To ascertain whether or not hsps play any role in the destabilization of alpha-amylase mRNA or in the delamellation process of ER, heat shocked cells were treated with the transcription inhibitor cordycepin, which effectively inhibits the synthesis of hsps yet does not affect alpha-amylase synthesis after this enzyme has been fully induced by gibberellic acid (12 hours). In the absence of hsp expression, heat shock still causes the destabilization of alpha-amylase mRNA and the delamellation of ER. Alternatively, the synthesis of hsps may be induced in the absence of temperature increase by incubating cells in the presence of arsenite. Arsenite-induced expression of some hsps in the absence of increased temperature does not result in the destabilization of alpha-amylase mRNA or in the delamellation of ER. If cordycepin or cycloheximide are used to inhibit hsp synthesis during heat shock, the tissue recovers from heat shock with normal recovery kinetics. Although hsps have been implicated in the establishment of thermotolerance, our observations indicate that hsps do not play a role in the other heat shock-induced changes observable in aleurone cells. Furthermore, if the synthesis of hsp mRNA is inhibited during heat shock (by cordycepin) hsp mRNAs are synthesized later, during recovery, indicating that there is a stable inducer of hsp synthesis in aleurone tissues.

Journal Article↗
PubMed2003

Metabolic heat production, heat loss and the circadian rhythm of body temperature in the rat.

Metabolic heat production (calculated from oxygen consumption), dry heat loss (measured in a calorimeter) and body temperature (measured by telemetry) were recorded simultaneously at 6 min intervals over five consecutive days in rats maintained in constant darkness. Robust circadian rhythmicity (confirmed by chi square periodogram analysis) was observed in all three variables. The rhythm of heat production was phase-advanced by about half an hour in relation to the body temperature rhythm, whereas the rhythm of heat loss was phase-delayed by about half an hour. The balance of heat production and heat loss exhibited a daily oscillation 180 deg out of phase with the oscillation in body temperature. Computations indicated that the amount of heat associated with the generation of the body temperature rhythm (1.6 kJ) corresponds to less than 1 % of the total daily energy budget (172 kJ) in this species. Because of the small magnitude of the fraction of heat balance associated with the body temperature rhythm, it is likely that the daily oscillation in heat balance has a very slow effect on body temperature, thus accounting for the 180 deg phase difference between the rhythms of heat balance and body temperature.

Animals↗
PubMed1997

Occurrence of a Highly Heat-Sensitive Spore Subpopulation of Bacillus coagulans STCC 4522 and Its Conversion to a More Heat-Stable Form.

The profile of the survival curves, at different heating temperatures, of B. coagulans STCC 4522 sporulated at 52(deg)C has been studied, focusing on the early moments of treatment. A highly heat-sensitive spore subpopulation that includes more than 90% of the total spore population has been found. This heat-sensitive spore fraction was inactivated after 2 s of treatment at 111(deg)C. Its heat resistance was as much as 200-fold lower than that of the heat-resistant spore fraction (D(inf111(deg)C) of 0.01 min for the heat-sensitive spore fraction compared with D(inf111(deg)C) of 2 min for the heat-resistant fraction). The shape of the survival curve at 108.5(deg)C was modified after a sublethal heat shock at 80(deg)C for 3.5 h, resulting in a straight-line survival curve. The temperature of treatment also influenced the shape of the survival curves. The conversion of the highly heat-sensitive spore subpopulation to a more heat-stable form is discussed.

Journal Article↗
PubMed1999

Evaluation of hand and finger heat loss with a heated hand model.

A heated full-scale hand model has been used to determine indirectly hand and finger heat losses of human subjects exposed to four ambient cold conditions (0, 4, 10 and 16 degrees C, air velocity approximately 0.3 m/s). Heat transfer coefficients determined with the hand model, were used to calculate heat flux based on measured skin to ambient temperature gradients. The responses of eight subjects from a previous study were used for the analysis. The measurements were carried out in a small climate chamber which was cooled by evaporating liquid carbon dioxide. The thermal hand was put into the chamber in a vertical position with the thumb up. The surface temperature of the thermal hand was controlled at 21, 25, 28, 31 and 34 degrees C under each of the four ambient cold conditions, in order to investigate possible temperature dependence of the calculated combined convective and radiate heat transfer coefficient (hCR). The value of hCR varied between approximately 9-13 W/m2 degree C for fingers and palm and back of hand, respectively. Calculated heat losses showed significant individual variation, corresponding to the maintained skin to ambient temperature gradient. Individual values from about 50 to more than 300 W/m2 were calculated. Several subjects showed CIVD and heat fluxes associated with this phenomenon were sometimes doubled. The measurement results showed realistic and comparable with literature date. The advantages of the thermal hand model can be counted as easy to use; directly measures the heat loss; highly reproducible and no interruption. It appears that a heated hand model provides a useful methods for analysis and quantification of hand heat loss.

Body Temperature Regulation↗
PubMedDate not supplied

Winner of the Lund Science Award 1992. Thermosensitization induced by step-down heating. A review on heat-induced sensitization to hyperthermia alone or hyperthermia combined with radiation.

A few minute's exposure to a high temperature (sensitizing treatment, ST) may substantially increase the cytotoxic and the radiosensitizing effect of a subsequent heating at a lower temperature (test treatment, TT). This phenomenon, which is known as step-down heating (SDH) or thermosensitization, has been observed both in cultured cells in vitro and in tumours and normal tissues in vivo. The effect of SDH increases with a lowering of TT temperature, but it is rapidly lost at temperatures very close to 37 degrees C. SDH-induced thermosensitization decays within a few hours, when an interval is inserted between ST and TT. In vitro results suggest an exponential decay of the SDH effect with half times ranging from 1.5- to 3.1 h. The effect of SDH increases with increasing ST time or temperature. For single heating, the Arrhenius plot is biphasic with activation energies of 500-800 and 1200-1700 kJ/mol above and below a break point temperature in the region 42.5-43.0 degrees C, respectively. For SDH, the Arrhenius plot gradually becomes monophasic with increasing severity of ST and it approaches asymptotically to an activation energy of about 400 kJ/mol. The reduction of the activation energy depends on cell survival after the priming ST and not on the specific ST heating time or temperature. SDH strongly enhances hyperthermic radiosensitization with a 5-6-fold reduction of the radiation dose required to achieve tumour control. The thermosensitizing and the radiosensitizing effects of SDH have several features in common. Both effects become more prominent when the TT temperature is decreased and when the ST heating time or temperature increases. In addition, the decay kinetics for both effects are comparable. For heat alone, the effect of SDH in tumour and normal tissue seems to be quantitatively similar. However, the therapeutic ratio may be increased by combining SDH with radiation. Biologically, the critical subcellular targets involved in the SDH effect have not been revealed. However, the ability of SDH to inhibit the clearance of heat-induced aggregation of proteins in the nucleus is interesting. Blockage of the nuclear function by proteins is a central theory in the present molecular biological models for both cell kill by heat and heat radiosensitization. Clinically, SDH may be an advantage since even a short exposure to high temperature increases the effect of an otherwise inadequate heat treatment. The disadvantages are that SDH complicates thermal dose calculations, and may cause unacceptable damage to normal tissue.

Animals↗
PubMed2003

Individual differences in self-reported heat tolerance. Is there a link to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat?

AIM: Tolerance to exercise in heat exhibits great interindividual variability. We questioned whether individual differences in self-reported heat tolerance within a group of endurance trained athletes are linked to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat. METHODS: Using a rating scale to assess the individual degree of tolerance to exercise in heat we allocated 12 non-heat-acclimated trained runners into two groups of 5 highly heat tolerant (HHT) and 7 less heat tolerant (LHT) athletes. Both groups performed a 60-min treadmill run (velocity 90% of individual anaerobic threshold, room temperature and humidity 28 inverted exclamation mark C and 50%, respectively). RESULTS: Sweating rate did not differ between HHT (mean +/- SEM: 0.44+/-0.02) and LHT (0.40+/-0.02 ml x kg(-1) x min(-1)). Compared to LHT, exercise-induced rises in core temperature (39.3+/-0.2/40.0+/-0.2 inverted exclamation mark C), heart rate, plasma norepinephrine and cortisol were significantly lower in HHT, while epinephrine did not exhibit differences between the groups. In contrast, response of human growth hormone (hGH) was significantly more pronounced in HHT. CONCLUSION: Our initial results, obtained in a small group of endurance-trained runners, show that self-reported tolerance to exercise in heat is associated with an attenuated rise in body core temperature during prolonged exercise under elevated ambient temperatures. This finding in heat tolerant athletes is paralleled by a lower stress response as reflected by lower rises in heart rate and stress hormones such as norepinephrine and cortisol. The functional significance (i.e. with respect to sweating function) of the more pronounced response of hGH in heat tolerant athletes warrants further research.

Body Temperature↗
PubMed1985

Optimal siting of heat flux transducers for the assessment of body heat loss when immersed in water.

Regional heat flux (intensity of heat flow rate, W m-2) was measured using heat flux transducers affixed to the skin surface at 14 sites on the left arm and 15 sites on both the left leg and the trunk (total of 44 locations) of human subjects during head-out immersion in water at temperatures between 11 and 28 degrees C. The heat flux data and skin temperature data were collected continuously over a 30-min period taking approximately 2.5 min to scan through all transducers in sequence before repeating the process. There were 3 immersions per individual, monitoring the arm or the leg or the trunk. The local measurements of heat flux from each of the body segments were summated and meaned to obtain a value of overall flux for each area of the body for each 2- to 3-min interval. This mean value was taken as the optimal value (Hopt) for any particular body segment. Every permutation of the positions of any 1, 2, 3, 4, or 5 heat flux transducers from the possible 14 or 15 sites was used to obtain a mean value which could be compared to the Hopt over the total duration of each immersion. Comparisons could be made between the best individual sites (Iopt) and Hopt as well as between the overall best site for the group of 10 people (Gopt) and Hopt. All possible permutations could be ranked in ascending order of preference based on a decreasing sum of the squares of the differences between Hopt and either Iopt or Gopt. Confirmation of the validity of this simple ranking system was based on an analysis of the percentage differences between Iopt or Gopt and Hopt. Such an analysis indicated that the better choice of discs when using a small number of transducers was between 3 and 5 sites, affording both reasonable accuracy and practicality. It is recommended that between 3 and 5 discs be used per body segment at specific locations and the calculated heat loss from each segment be weighted according to its area of representation to give a value for the mean rate of total body heat loss. A reasonable level of accuracy was demonstrated using Gopt permutations for measuring both the rate of heat flow as well as the integral of the data to obtain a value of the quantity of heat (Joules) lost from the body.

Adult↗
PubMed1996

The heat shock factor and mitochondrial Hsp70 are necessary for survival of heat shock in Saccharomyces cerevisiae.

A heat shock recovery assay on solid medium (Nwaka et al. (1995) J. Biol. Chem. 270, 10193-10198) as well as the classical cell counting method were used to investigate the function of some heat shock proteins in thermotolerance. We show that expression of intact heat shock factor protein (HSF), which regulates the stress induced expression of heat shock proteins (HSPs), is necessary for recovery from heat shock. A HSF1 mutant (hsf1-m3) which does not induce the expression of some heat shock proteins at heat stress (37-40 degrees C) is defective in recovery after heat shock at 50-52 degrees C compared to a corresponding wild-type strain in both stationary and exponentially growing cells. Using two temperature sensitive mutants of the mitochondrial Hsp70 (ssc1-2 and ssc1-3) encoded by the SSC1 gene, we show that the ssc1-3 mutant, which has a mutation in the ATPase domain, is defective in recovery after heat shock in contrast to the ssc1-2 mutant, which has a mutation in the peptide binding domain. Different binding capacities for unfolded proteins are shown to be the molecular reason for the observed phenotypes. The thermotolerance defect of the hsf1-m3 and ssc1-3 mutants is demonstrated for both glucose and glycerol media.

Adaptation, Physiological↗
PubMed1996

The Bradyrhizobium japonicum rpoH1 gene encoding a sigma 32-like protein is part of a unique heat shock gene cluster together with groESL1 and three small heat shock genes.

The heat shock response of Bradyrhizobium japonicum is controlled by a complex network involving two known regulatory systems. While some heat shock genes are controlled by a highly conserved inverted-repeat structure (CIRCE), others depend on a sigma 32-type heat shock sigma factor. Using Western blot (immunoblot) analysis, we confirmed the presence of a sigma 32-like protein in B. japonicum and defined its induction pattern after heat shock. A B. japonicum rpoH-like gene (rpoH1) was cloned by complementation of an Escherichia coli strain lacking sigma 32. A knockout mutation in rpoH1 did not abolish sigma 32 production in B. japonicum, and the rpoH1 mutant showed the wild-type growth phenotype, suggesting the presence of multiple rpoH homologs in this bacterium. Further characterization of the rpoH1 gene region revealed that the rpoH1 gene is located in a heat shock gene cluster together with the previously characterized groESL1 operon and three genes encoding small heat shock proteins in the following arrangement: groES1, groEL1, hspA, rpoH1, hspB, and hspC. Three heat-inducible promoters are responsible for transcription of the six genes as three bicistronic operons. A sigma 32-dependent promoter has previously been described upstream of the groESL1 operon. Although the hspA-rpoH1 and hspBC operons were clearly heat inducible, they were preceded by sigma 70-like promoters. Interestingly, a stretch of about 100 bp between the transcription start site and the start codon of the first gene in each of these two operons was nearly identical, making it a candidate for a regulatory element potentially allowing heat shock induction of sigma 70-dependent promoters.

Amino Acid Sequence↗
PubMed1996

Thermotolerance attenuates heat-induced increases in [Ca2+]i and HSP-72 synthesis but not heat-induced intracellular acidification in human A-431 cells.

BACKGROUND: Thermotolerance affects cell viability, retards translation of heat shock proteins, and protects RNA slicing mechanisms. We reported previously that heat shocking nonthermotolerant cells causes an intracellular acidification and an increase in cytosolic free Ca2+ ([Ca2+]i) in addition to an induction of heat shock protein 72kDa (HSP-72) production. This study characterized heat-induced changes in cytosolic Ca2+, H+, and HSP-72 synthesis in thermotolerant A-431 cells. METHODS: We studied heat-induced changes in pH(i), [Ca2+]i, and HSP-72 using thermotolerant A-431 cell monolayers. pH(i) and [Ca2+]i were determined using fluorescence probes, and HSP-72 was measured by SDS-PAGE. The mRNA encoding HSP-72 was measured by Northern blots probed with a [32P]-labeled 2.3 kb fragment of an HSP-70 cDNA insert. RESULTS: Heat shocking thermotolerant cells induced the same degree of intracellular acidification as that induced in nonthermotolerant cells, but the heat-induced increase in [Ca2+]i was less in thermotolerant cells. This diminished response was characterized by an increase in Km for external Ca2+ and was blocked by pretreatment with cycloheximide, indicating a newly synthesized protein is involved. Similar to what was seen in nonthermotolerant cells, the heat-induced increase in [Ca2+]i in thermotolerant cells depended on external Na+ concentration and was blocked by dichlorobenzamil, though thermotolerant cells were more sensitive to the inhibitor (IC50 = 0.21 mumol/L for nonthermotolerant, 0.025 mumol/Lm for thermotolerant). Thermotolerant cells contained high resting levels of HSP-72. Heat shocking these cells attenuated the HSF translocation from cytosol to nucleus and did not induce a further synthesis of HSP-72 mRNA and protein. CONCLUSIONS: The results suggest that thermotolerance desensitizes the machinery required for Ca2+ entry. Low [Ca2+]i levels probably result in diminished HSP-72 mRNA production and less HSP-72 synthesis.

Acclimatization↗
PubMed2005

Small heat shock proteins are differentially regulated during pollen development and following heat stress in tobacco.

In plants small heat shock proteins (sHsp) are abundantly expressed upon heat stress in vegetative tissue, however, sHsp expression is also developmentally induced in pollen. The developmental induction of sHsp has been related to the potential for stress-induced microspore embryogenesis. We investigated the polymorphism among sHsp and their expression during pollen development and after heat stress in tobacco. Real-time RT-PCR was used for quantification of mRNA of two known and nine newly isolated cDNAs representing cytosolic sHsp. At normal temperature most of these genes are not transcribed in vegetative tissues, however, all genes were expressed during pollen development. Low levels of mRNAs were found for sHsp-1A and -1B in early-unicellular stage, increasing four to sevenfold in mature pollen. Nine other genes are up-regulated in unicellular and down-regulated in bicellular pollen; three these genes show stage-specific expression. Western analysis revealed that cytosolic class I and II sHsp are developmentally expressed during all stages of pollen development. Different subsets of cytosolic sHsp genes are expressed in a stage-specific fashion suggesting that certain sHsp genes may play specific roles in early, others during later stages of pollen development. Heat stress results in a relatively weak and incomplete response in pollen: (i) the heat-induced levels of mRNA (excepting sHsp-2B, -3C and -6) are much lower than in leaves, (ii) several sHsp are not detected after heat stress in pollen, although, they are heat-inducibly expressed in leaves. Application of heat stress, cold, and starvation, which induce microspore embryogenesis, modify mRNA levels and the patterns of 2-D-separated sHsp, but only heat stress enhances the expression of sHsp in microspores. There is no correlation of the expression of specific sHsp with the potential for microspore embryogenesis.

Amino Acid Sequence↗