Production Of Heat Shock Proteins Research Articles

Enzymatic antioxidants in response to methyl jasmonate and salicylic acid and their effect on chilling tolerance in lemon fruit [Citrus limon (L.) Burm. F.

To prevent excessive accumulation of reactive oxygen species (ROS), as typically occurs during cold storage, fruit have evolved antioxidant defence mechanisms, such as the production of heat shock proteins (HSPs), that reduce chilling injury (CI). It was hypothesised that treatments with methyl jasmonate (MJ) and salicylic acid (SA) may enhance chilling tolerance in lemon fruit by inducing the production of enzymatic antioxidants. Fully mature lemon fruit were sourced from three production sites with varying climate: moderate subtropical (New Venture Farm), warm temperate (Tala Valley Citrus Estate) and cool subtropical conditions (Sun Valley Estate). The fruit were treated with MJ and SA, waxed and stored at −0.5, 2, or 4.5°C for 28days plus 7days at 23°C. The manifestation of CI and changes in ROS, as well as in enzymatic antioxidant systems, such as catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR), as well as HSPs were investigated in lemon flavedo. Symptoms of CI were more severe in control fruit stored at 4.5°C than at 2 or −0.5°C. Fruit sourced from the moderate subtropical and warm temperate locations had higher enzymatic antioxidant activities (CAT, APX and GR), a higher HSPs expression and a lower accumulation of ROS than those sourced from the cool subtropical location. Treatment with 10μMMJ plus 2mM SA reduced CI, suppressed ROS production, increased CAT, APX and GR activity, and enhanced the accumulation of HSPs, suggesting that enzymatic antioxidants and HSPs are involved in conveying chilling tolerance to MJ- and SA-treated lemon fruit. The increase in activity of these antioxidant enzymes, together with HSPs, could be part of the mode of action by which MJ and SA convey chilling tolerance to lemon fruit.

Heavy metal-induced oxidative stress on seed germination and seedling development: a critical review.

Heavy metal contamination in soils can influence plants and animals, often leading to toxicosis. Heavy metals can impact various biochemical processes in plants, including enzyme and antioxidant production, protein mobilization and photosynthesis. Hydrolyzing enzymes play a major role in seed germination. Enzymes such as acid phosphatases, proteases and α-amylases are known to facilitate both seed germination and seedling growth via mobilizing nutrients in the endosperm. In the presence of heavy metals, starch is immobilized and nutrient sources become limited. Moreover, a reduction in proteolytic enzyme activity and an increase in protein and amino acid content can be observed under heavy metal stress. Proline, is an amino acid which is essential for cellular metabolism. Numerous studies have shown an increase in proline content under oxidative stress in higher plants. Furthermore, heat shock protein production has also been observed under heavy metal stress. The chloroplast small heat shock proteins (Hsp) reduce photosynthesis damage, rather than repair or help to recover from heavy metal-induced damage. Heavy metals are destructive substances for photosynthesis. They are involved in destabilizing enzymes, oxidizing photosystem II (PS II) and disrupting the electron transport chain and mineral metabolism. Although the physiological effects of Cd have been investigated thoroughly, other metals such as As, Cr, Hg, Cu and Pb have received relatively little attention. Among agricultural plants, rice has been studied extensively; additional studies are needed to characterize toxicities of different heavy metals on other crops. This review summarizes the current state of our understanding of the effects of heavy metal stress on seed germination and seedling development and highlights informational gaps and areas for future research.

Protective Effect of Camellia Oil (Camellia oleifera Abel.) against Ethanol-Induced Acute Oxidative Injury of the Gastric Mucosa in Mice.

Camellia oil, a common edible oil in Taiwan and China, has health effects for the gastrointestinal tract in folk medicine, and it contains abundant unsaturated fatty acids and phytochemicals. However, the preventive effect of camellia oil on ethanol-induced gastric ulcers remains unclear. This study was aimed to evaluate the preventive effect of camellia oil on ethanol-induced gastric injury in vitro and in vivo as well as its mechanisms of action. In an in vitro study, our results showed that pretreatment of RGM-1 cells with camellia oil enhanced the migration ability as well as increased heat shock protein expression and reduced apoptotic protein expression. In animal experiments, mice pretreated with camellia oil effectively showed improved ethanol-induced acute injury of the gastric muscosa and oxidative damage through the enhancement of antioxidant enzyme activities and heat shock protein and PGE2 production, as well as the suppression of lipid peroxidation, apoptosis-related proteins, pro-inflammatory cytokines, and NO production. Histological injury score and hemorrhage score in ethanol-induced gastric mucosal damage dramatically elevated from the control group (0.00 ± 0.0) to 3.40 ± 0.7 and 2.60 ± 0.5, respectively. However, treatments with camellia oil or olive oil (2 mL/kg bw) and lansoprazole (30 mg/kg bw) showed significant decreases in elevation of injury score and hemorrhage score (p < 0.05). Therefore, camellia oil has the potential to ameliorate ethanol-induced acute gastric mucosal injury through the inhibition of inflammation and oxidative stress.

Upregulation of heat-shock proteins in larvae, but not adults, of the flesh fly during hot summer days.

Heat-shock proteins (HSPs) are highly expressed when organisms are exposed to thermal stresses. The HSPs are considered to play significant roles in thermal adaptation because they function as molecular chaperones facilitating proper protein synthesis. The expression of HSPs under field conditions, however, has not been evaluated much, and their importance, based on the ecological contexts in nature, is still unclear. We investigated this aspect in the larvae and adults of the flesh fly, Sarcophaga similis. These larvae spend their larval life in the carrion or faeces of vertebrates; therefore, they are less mobile and are occasionally exposed to high temperature. In contrast, the adults of this species can fly and, therefore, they are highly mobile. Massive transcription of Hsps was detected both in the larvae and adults in a laboratory heat-shock experiment. The larvae in the field showed no or less Hsp production on thermally mild days, whereas considerable upregulation of Hsp expression was detected on days with high temperature. The adults can also be exposed to thermal stress as high as 40°C or higher in the field. However, most of the flies showed no or less Hsp expression. The observations in the experimental cage under field conditions revealed behavioural thermoregulation of adults through microhabitat selection. The present study demonstrates ontogenetic alteration of the strategy to overcome thermal stress in an insect; in the field, less mobile larvae use physiological protection against heat (HSP production), whereas highly mobile adults avoid the stress behaviourally (through microhabitat selection).

Regulation of heat-shock genes in bacteria: from signal sensing to gene expression output.

The heat-shock response is a mechanism of cellular protection against sudden adverse environmental growth conditions and results in the prompt production of various heat-shock proteins. In bacteria, specific sensory biomolecules sense temperature fluctuations and transduce intercellular signals that coordinate gene expression outputs. Sensory biomolecules, also known as thermosensors, include nucleic acids (DNA or RNA) and proteins. Once a stress signal is perceived, it is transduced to invoke specific molecular mechanisms controlling transcription of genes coding for heat-shock proteins. Transcriptional regulation of heat-shock genes can be under either positive or negative control mediated by dedicated regulatory proteins. Positive regulation exploits specific alternative sigma factors to redirect the RNA polymerase enzyme to a subset of selected promoters, while negative regulation is mediated by transcriptional repressors. Interestingly, while various bacteria adopt either exclusively positive or negative mechanisms, in some microorganisms these two opposite strategies coexist, establishing complex networks regulating heat-shock genes. Here, we comprehensively summarize molecular mechanisms that microorganisms have adopted to finely control transcription of heat-shock genes.

Translation of heat shock proteins is regulated by poly(A)‐binding protein assembly

How do cells sense and respond to changes in the environment? During heat stress, numerous eukaryotic RNA and protein species assemble into macromolecular bodies ‐ stress granules ‐ the function of which is largely unknown. Simultaneously, cells increase transcription of genes encoding heat shock proteins, many of which are molecular chaperones. In addition to increased transcription, the mRNA for these genes is also translated more efficiently. Thus, heat shock protein production is regulated by both transcription and translation. These heat‐induced mRNAs have exceptionally A‐rich 5′ untranslated regions (UTRs), which have long been known to mediate cap‐independent translation. We observe that poly(A)‐binding protein (PABP, Pab1 in S. cerevisiae) is bound to these A‐rich UTRs during exponential growth. Pab1 is able to repress translation of its own mRNA by binding a similar A‐rich UTR. We find that Pab1 represses translation of mRNA by binding A‐rich UTRs of heat shock proteins. Further, we propose that during heat‐shock, as Pab1 assembles into heat‐induced RNA‐protein granules, Pab1 releases bound 5′ UTRs, and relieves repression. We have recapitulated Pab1‐mediated repression and heat‐induced relief with an in vitro translation system. Moreover, yeast expressing assembly‐impaired Pab1 are not able to grow at elevated temperature; this result is consistent with disruption of an assembly‐mediated regulatory mechanism. Viewed through this lens, formation of RNA‐protein granules is a regulatory response, whose functions include translational regulation.Support or Funding InformationThe molecular and cellular biology training grant T32 GM007183

Antipsychotics promote GABAergic interneuron genesis in the adult rat brain: Role of heat-shock protein production

Current antipsychotics reduce positive symptoms and reverse negative symptoms in conjunction with cognitive behavioral issues with the goal of restoring impaired occupational and social functioning. However, limited information is available on their influence on gliogenesis or their neurogenic properties in adult schizophrenia brains, particularly on GABAergic interneuron production. In the present study, we used young adult subventricular zone (SVZ)-derived progenitor cells expressing proteoglycan NG2 cultures to examine the oligodendrocyte and GABAergic interneuron genesis effects of several kinds of antipsychotics on changes in differentiation function induced by exposure to the NMDA receptor antagonist MK-801. We herein demonstrated that antipsychotics promoted or restored changes in the oligodendrocyte/GABAergic interneuron differentiation functions of NG2(+) cells induced by the exposure to MK-801, which was considered to be one of the drug-induced schizophrenia model. We also demonstrated that antipsychotics restored heat-shock protein (HSP) production in NG2(+) cells with differentiation impairment. The antipsychotics olanzapine, aripiprazole, and blonanserin, but not haloperidol increased HSP90 levels, which were reduced by the exposure to MK-801. Our results showed that antipsychotics, particularly those recently synthesized, exerted similar GABAergic interneuron genesis effects on NG2(+) neuronal/glial progenitor cells in the adult rat brain by increasing cellular HSP production, and also suggest that HSP90 may play a crucial role in the pathophysiology of schizophrenia and is a key target for next drug development.

Mechanisms Explaining Muscle Fatigue and Muscle Pain in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a Review of Recent Findings.

Here, we review potential causes of muscle dysfunction seen in many patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) such as the effects of oxidative and nitrosative stress (O&NS) and mitochondrial impairments together with reduced heat shock protein production and a range of metabolic abnormalities. Several studies published in the last few years have highlighted the existence of chronic O&NS, inflammation, impaired mitochondrial function and reduced heat shock protein production in many patients with ME/CFS. These studies have also highlighted the detrimental effects of chronically elevated O&NS on muscle functions such as reducing the time to muscle fatigue during exercise and impairing muscle contractility. Mechanisms have also been revealed by which chronic O&NS and or impaired heat shock production may impair muscle repair following exercise and indeed the adaptive responses in the striated muscle to acute and chronic increases in physical activity. The presence of chronic O&NS, low-grade inflammation and impaired heat shock protein production may well explain the objective findings of increased muscle fatigue, impaired contractility and multiple dimensions of exercise intolerance in many patients with ME/CFS.

Modulation of the heat shock response is associated with acclimation to novel temperatures but not adaptation to climatic variation in the ants Aphaenogaster picea and A. rudis

Ecological diversification into thermally divergent habitats can push species toward their physiological limits, requiring them to accommodate temperature extremes through plastic or evolutionary changes that increase persistence under the local thermal regime. One way to withstand thermal stress is to increase production of heat shock proteins, either by maintaining higher baseline abundance within cells or by increasing the magnitude of induction in response to heat stress. We evaluated whether environmental variation was associated with expression of three heat shock protein genes in two closely-related species of woodland ant, Aphaenogaster picea and A. rudis. We compared adult workers from colonies collected from 25 sites across their geographic ranges. Colonies were maintained at two different laboratory temperatures, and tested for the independent effects of environment, phylogeny, and acclimation temperature on baseline and heat-induced gene expression. The annual maximum temperature at each collection site (Tmax) was not a significant predictor of either baseline expression or magnitude of induction of any of the heat shock protein genes tested. A phylogenetic effect was detected only for basal expression of Hsp40, which was lower in the most southern populations of A. rudis and higher in a mid-range population of possible hybrid ancestry. In contrast, a higher acclimation temperature significantly increased baseline expression of Hsc70-4, and increased induction of Hsp40 and Hsp83. Thus, physiological acclimation to temperature variation appears to involve modulation of the heat shock response, whereas other mechanisms are likely to be responsible for evolutionary shifts in thermal performance associated with large-scale climate gradients.

Hepatitis C Virus E2 Protein Induces Upregulation of IL-8 Pathways and Production of Heat Shock Proteins in Human Thyroid Cells.

Thyroiditis is one of the most common extrahepatic manifestations of hepatitis C virus (HCV) infection. By binding to surface cell receptor CD81, HCV envelope glycoprotein E2 mediates entry of HCV into cells. Studies have shown that different viral proteins may individually induce host responses to infection. We hypothesized that HCV E2 protein binding to CD81 expressed on thyroid cells activates a cascade of inflammatory responses that can trigger autoimmune thyroiditis in susceptible individuals. Human thyroid cell lines ML-1 and human thyrocytes in primary cell culture were treated with HCV recombinant E2 protein. The expression of major proinflammatory cytokines was measured at the messenger RNA and protein levels. Next-generation transcriptome analysis was used to identify early changes in gene expression in thyroid cells induced by E2. HCV envelope protein E2 induced strong inflammatory responses in human thyrocytes, resulting in production of interleukin (IL)-8, IL-6, and tumor necrosis factor-α. Furthermore, the E2 protein induced production of several heat shock proteins including HSP60, HSP70p12A, and HSP10, in human primary thyrocytes. In thyroid cell line ML-1, RNA sequencing identified upregulation of molecules involved in innate immune pathways with high levels of proinflammatory cytokines and chemokines and increased expression of costimulatory molecules, specifically CD40, known to be a major thyroid autoimmunity gene. Our data support a key role for HCV envelope protein E2 in triggering thyroid autoimmunity through activation of cytokine pathways by bystander mechanisms.

Different Relationship between hsp70 mRNA and hsp70 Levels in the Heat Shock Response of Two Salmonids with Dissimilar Temperature Preference

The heat shock response (HSR) refers to the rapid production of heat shock proteins (hsps) in response to a sudden increase in temperature. Its regulation by heat shock factors is a good example of how gene expression is transcriptionally regulated by environmental stresses. In contrast, little is known about post-transcriptional regulation of the response. The heat shock response is often used to characterize the temperature tolerance of species with the rationale that whenever the response sets on, a species is approaching its lethal temperature. It has commonly been considered that an increase in hsp mRNA gives an accurate indication that the same happens to the protein level, but this need not be the case. With climate change, understanding the effects of temperature on gene expression of especially polar organisms has become imperative to evaluate how both biodiversity and commercially important species respond, since temperature increases are expected to be largest in polar areas. Here we studied the HSR of two phylogenetically related Arctic species, which differ in their temperature tolerance with Arctic charr having lower maximally tolerated temperature than Atlantic salmon. Arctic charr acclimated to 15°C and exposed to 7°C temperature increase for 30 min showed both an increase in hsp70 mRNA and hsp70 whereas in salmon only hsp70 mRNA increased. Our results indicate that the temperature for transcriptional induction of hsp can be different from the one required for a measurable change in inducible hsp level. The species with lower temperature tolerance, Arctic charr, are experiencing temperature stress already at the higher acclimation temperature, 15°C, as their hsp70 mRNA and hsp70 levels were higher, and they grow less than fish at 8°C (whereas for salmon the opposite is true). Consequently, charr experience more drastic heat shock than salmon. Although further studies are needed to establish the temperature range and length of exposure where hsp mRNA and hsp level are disconnected, the observation suggests that by measuring both hsp mRNA and hsp level, one can evaluate if a species is approaching the higher end of its temperature tolerance, and thus evaluate the vulnerability of an organism to the challenges imposed by elevated water temperature.

Non-lethal heat shock increases tolerance to metal exposure in brine shrimp

Pollution and temperature increase are two of the most important stressors that aquatic organisms are facing. Exposure to elevated temperatures and metal contamination both induce heat shock proteins (HSPs), which may thus be involved in the induced cross-tolerance in various organisms. This study aimed to test the hypothesis that exposure to a non-lethal heat shock (NLHS) causes an increased tolerance to subsequent metal exposure. Using gnotobiotic cultures of the brine shrimp Artemia franciscana, the tolerance to Cd and Zn acute exposures was tested after a prior NLHS treatment (30min exposure to 37°C). The effects of NLHS and metal exposure were also assessed by measuring 70kDa-HSPs production, along with the analysis of epigenetic markers such as DNA methylation and histone H3 and histone H4 acetylation. Our results showed that heat-shocked Artemia had increased acute tolerance to Cd and Zn. However, different patterns of HSPs were observed between the two metal compounds and no epigenetic alterations were observed in response to heat shock or metal exposure. These results suggest that HSP production is a phenotypically plastic trait with a potential role in temperature-induced tolerance to metal exposure.

Response and Tolerance Mechanism of Cotton Gossypium hirsutum L. to Elevated Temperature Stress: A Review.

Cotton is an important multipurpose crop which is highly sensitive to both biotic and abiotic stresses. Proper management of this cash crop requires systematic understanding of various environmental conditions that are vital to yield and quality. High temperature stress can severely affect the viability of pollens and anther indehiscence, which leads to significant yield losses. Cotton can respond to withstand adverse environmental condition in several phases among which the accumulation of chemicals is extremely vital. Calcium, kinases, reactive oxygen species, carbohydrate, transcription factors, gene expression regulation, and plant hormones signaling pathways are playing a handy role in activating the major genes responsible to encounter and defend elevated temperature stress. The production of heat shock proteins is up-regulated when crops are unleashed to high temperature stress. Molecular breeding can play a functional role to identify superior genes for all the important attributes as well as provide breeder ready markers for developing ideotypes. The development of high-temperature resistant transgenic cultivars of cotton can grant a stability benefit and can also ameliorate the production capacity in response to elevated temperature.

Clam mitochondria respond better to hypoxia than scallop mitochondria

Few terrestrial animals ever experience hypoxia (when oxygen is scarce), but spells of low oxygen availability are routine for creatures clinging to life on the seashore: ‘Diurnal cycles of respiration and photosynthesis in the coastal zones commonly lead to O2 swings from near-anoxia during the night to hyperoxia during the day’, says Inna Sokolova from the University of North Carolina at Charlotte, USA. Yet, many of these creatures can withstand periods of oxygen deprivation lasting weeks and even months. Sokolova explains that several of the mechanisms that underpin the coast dwellers’ survival are already known, including the use of alternative mechanisms to generate ATP and the animals’ ability to drop their metabolic rate to conserve energy. However, Sokolova explains that little was known about how these resilient species protected the essential mitochondria – which consume oxygen to generate ATP – from the damaging effects of oxygen deprivation.Sokolova and a team of colleagues investigated the function of mitochondria in two shoreline species: the hypoxia-tolerant hard clam (Mercenaria mercenaria), which can survive for 2 weeks with no oxygen at all, and the less robust bay scallop (Argopecten irradians), which can only survive a few hours in anoxia. Keeping the bivalves in deoxygenated water (less than 0.1% oxygen) for 18 h, the team then collected samples from the gills, hepatopancreas tissue and adductor muscles to find out how the mitochondria had responded to oxygen deprivation. In addition, the team collected tissues from molluscs that had not experienced hypoxia, and from molluscs that had been transferred back into water with normal oxygen concentrations after hypoxia to find out how they responded as damaging oxygen flooded back into their bodies.Analysing the animals’ responses, the team saw that when the oxygen returned after an extended period of hypoxia, the scallops suffered similar experiences to those of other hypoxia-sensitive animals: the mitochondria were impaired, reducing their oxidation and phosphorylation capacities as they partially depolarized and the potential difference across the membrane reduced. In parallel, the vulnerable scallops ramped up production of heat shock proteins – which mop up proteins that have been damaged by the oxygen influx – in order to reduce the damage incurred by the mitochondria during reoxygenation. In contrast, the robust clams increased the oxidative capacity of their mitochondria during hypoxia and this also continued rising when the oxygen returned. Meanwhile, both of the molluscs reduced phosphorylation activity (which is normally responsible for ATP production via the Fo,F1-ATPase) during the extended period of hypoxia, ‘Likely to prevent ATP wastage by the reverse action of the ATPase’, say Sokolova and colleagues, although the clams regained this activity during the 1 h period of reoxygenation, when the scallops’ phosphorylation activity failed to improve. And when the team tested the bivalves’ ability to conserve energy by downregulating non-essential metabolic processes, it was clear that the clam was better able to reduce its energy expenditure than the more vulnerable scallop, although neither animal was severely energy deprived.So, a period of hypoxia dramatically affects both the hypoxia-tolerant hard clam and the more susceptible bay scallop, but alterations in the physiology of the clam leave it better prepared to tackle extended periods of hypoxia than its scallop shore-mate.

The Heat Stress Response and Diabetes: More Room for Mitochondrial Implication.

Heat preconditioning is a rapid cellular adaptive mechanism shared by many cells/ organs / organisms that results in synthesis and accumulation of heat shock proteins (HSPs), which are responsible for increased tolerance and survival of animals during and after heat stress (HS). HSPs function as molecular chaperones by restoring cellular homeostasis and promoting cell survival, and their major functions include protection of cells from injury by preventing protein damage and aggregation. Abundant evidence points to the ability of one kind of stress caused by external factors that induce primary adaptations in the organism to provide protection against additional stress of the same or another type, a phenomenon known as cross-tolerance. Diabetes mellitus (DM) is one of the diseases which have been associated with increased tissue sensitivity and vulnerability due to incorrect protein folding. Thus, HSPs may play an important role in minimizing the protein damage that can occur under the stressful conditions created by the disease. By increasing HSP production, heat preconditioning may be a promising therapy for patients with lifestylerelated diseases such as hypercholesterolemia, hypertension, DM and obesity. Also, pancreatic β-cells exposed to acute HS activate defence mechanisms which include HSP synthesis and are less sensitive to the effects of cytotoxic agents such as NO, oxygen radicals and β-cytotoxic diabetogenic agents, such as streptozotocin (STZ). Mitochondrial dysfunction and mitochondria-specific cell stress are associated and can even be a primary abnormality caused by DMinduced hyperglycaemia and oxidative stress. There are an increasing number of genetic and/or pharmacological modulations of HSPs that have revealed the connection between HSPs, mitochondria and diabetes. HSPs may affect mitochondrial function in multiple ways, but the influence on skeletal muscle and adipose tissue, as well as on the pancreas, has attracted most interest as a key element in the development of novel pharmacological approaches to treating DM and associated metabolic conditions.

Heat stress enhances LTM formation in Lymnaea: role of HSPs and DNA methylation.

Environmentally relevant stressors alter the memory-forming process in Lymnaea following operant conditioning of aerial respiration. One such stressor is heat. Previously, we found that following a 1 h heat shock, long-term memory (LTM) formation was enhanced. We also had shown that the heat stressor activates at least two heat shock proteins (HSPs): HSP40 and HSP70. Here, we tested two hypotheses: (1) the production of HSPs is necessary for enhanced LTM formation; and (2) blocking DNA methylation prevents the heat stressor-induced enhancement of LTM formation. We show here that the enhancing effect of the heat stressor on LTM formation occurs even if snails experienced the stressor 3 days previously. We further show that a flavonoid, quercetin, which inhibits HSP activation, blocks the enhancing effect of the heat stressor on LTM formation. Finally, we show that injection of a DNA methylation blocker, 5-AZA, before snails experience the heat stressor prevents enhancement of memory formation.

The isoquinoline alkaloid sanguinarine which inhibits chaperone activity enhances the production of heat shock proteins in Arabidopsis.

Sanguinarine is an isoquinoline alkaloid produced by Papaveraceae plants. Because sanguinarine has antimicrobial activity, it is believed to be related to the plants' chemical defense systems. However, its action against plants has not been well understood. A previous study reported that among 12 alkaloids, sanguinarine was the only compound which enhanced heat tolerance in Arabidopsis. Here we performed a promoter assay using a heat shock protein gene (HSP17.6C-CI) of Arabidopsis to assess the induction of heat shock responses by alkaloids. Although sanguinarine induced the heat shock response, the other 11 alkaloids did not. Sanguinarine promoted the production of HSP17.6C-CI protein, but berberine and papaverine, which are isoquinoline alkaloids as well as sanguinarine, did not promote it. It is known that geldanamycin, a small molecule chaperone inhibitor, activates the heat shock response in Arabidopsis. Although sanguinarine inhibited the chaperone activities of wheat germ extract much like geldanamycin, berberine and papaverine influenced the activities very little. These results suggest that sanguinarine may promote the heat shock response by regulating the chaperone activities in the way that geldanamycin does in plants.

English

Water scarcity is the most serious abiotic stress restricting plant productivity throughout the world. Losses in crop yield due to drought exceed from losses caused by other environmental factors. In this review article different morphological, physiological and yield attributes of cotton under drought stress, mechanism of drought induced losses and various management strategies to mitigate drought stress have been discussed. Drought stress reduces growth of leaf, stem and root, interferes with leaf water relations, photosynthesis, respiration, reduces water-use efficiency and ultimately yield of cotton. Under water deficit conditions cotton shows various responses to cope with drought stress. The major mechanisms include accumulation of osmoregulators, plant growth regulators and production of heat shock proteins. Different management strategies to alleviate water deficit stress like foliar application of osmolytes, potassium and growth regulators (hormones), various drought responsive genes, proteins at molecular level, screening and breeding programs against drought tolerance and mulching are also discussed in this paper.

Proper NMR methods for studying RNA thermometers

Abstract In some pathogenic bacteria, there are RNA thermometers, which regulate the production of virulence associated factors or heat shock proteins depending on temperature changes. Like a riboswitches, RNA thermometers are located in the 5’-untranslated region and involved translational gene regulatory mechanism. RNA thermometers block the ribosome-binding site and start codon area under the 37℃ living systems. within their secondary structure. After bacterial infection, increased the temperature in the host causes conformations changes of RNA, and the ribosome-binding site is exposed for translational initiation. Because structural differences between open and closed forms of RNA thermometers are mainly mediated by base pairing changes, NMR spectroscopy is a very useful method to study these thermodynamically changing RNA structure. In this review, we briefly provide a fundamental function of RNA thermometers, and also suggest a proper NMR experiments for studying RNA thermometers.

Sperm Storage in the Female Reproductive Tract.

The capacity for sperm storage within the female reproductive tract occurs widely across all groups of vertebrate species and is exceptionally well developed in some reptiles (maximum duration seven years) and fishes (maximum duration >1 year). Although there are many reports on both the occurrence of female sperm storage in diverse species and its adaptive benefits, few studies have been directed toward explaining the mechanisms involved. In this article we review recent findings in birds and mammals in an effort to develop hypotheses that could be translated into research applications in animal breeding technologies. There are pockets of evidence to suggest that the local epithelial cells, sometimes arranged as sperm storage tubules, can respond to spermatozoa by producing heat shock proteins as well as providing an environment rich in antioxidants. Moreover, the local immune system seems to tolerate the arrival of spermatozoa, while retaining the ability to combat the arrival of infectious microorganisms.