Molecular responses of plants to an increased incidence of heat shock

Abstract. Climatic change as a result of the greenhouse effect is widely predicted to increase mean temperatures globally and, in turn, increase the frequency with which plants are exposed to heat shock conditions, particularly in the semi-arid tropics. The consequences of extreme high-temperature treatments on plants have been considered, particularly in relation to the synthesis of heat shock proteins (HSPs) and the capacity to acquire thermotolerance. The heat shock response is described using results obtained with seedlings of the tropical cereals, sorghum ( Sorghum bicolor ) and pearl millet ( Pennisetum glaucum ). A gradual temperature increase, as would occur in the field, is sufficient to induce thermotolerance. The synthesis of HSPs is a transient phenomenon and ceases once the stress is released. Despite the persistence of the HSPs themselves, de novo synthesis of HSPs is required for the induction of thermotolerance each time high temperatures are encountered. The effect of a repeated, diurnal heat shock was investigated and genotypic differences found in the ability to induce the heat shock response repeatedly.     

The capacity of Drosophila to heat harden associates with low rates of heat-shocked protein synthesis

The thermotolerance of a species or of an ecotype is important for determining its habitat range and vigour, and considerable research has focused on identifying underlying physiological, biochemical and genetic bases of thermotolerance traits. Rates of protein synthesis in tissues when organisms experience a sudden heat stress as occurs on rare hot days may be important to avoid heat-induced paralysis and to survive. While natural variation in Drosophila melanogaster thermotolerance has been associated with heat-shock gene expression, little attention has been given to examining the thermo-protective role of protein synthesis generally. Using two independently derived sets of single-pair mating lines, we characterised variation in rates of protein synthesis in dissected ovarian tissues, both before and after a heat shock applied at different severities in the two sets. In both sets of lines heat-shocked protein synthesis rates were negatively associated with the increase in heat knockdown tolerance after hardening. These associations occurred in a different sex in each set. Variation in rates of Hsp70 synthesis failed to associate with levels of heat tolerance or general protein synthesis. Our results suggest heritable variation in the rate of protein synthesis following heat stress, independently of Hsp70 variation, contributes to heat tolerance variation in this species.     

Protective mechanisms of heat tolerance in crop plants

High temperature (HT) has become a global concern because it severely affects the growth and production of crops. Heat stress causes an abrupt increase in the expression of stress-associated proteins which provide tolerance by stimulating the defense response in plants. Heat-shock proteins (Hsps) and antioxidant enzymes are important in encountering heat stress in plants. The heat-shock response is characterized by repression of normal cellular protein synthesis and induction of Hsp synthesis. Under HT stress, upregulation of various enzymatic and nonenzymatic antioxidants, maintenance of cell membrane stability, production of various compatible solutes and hormonal changes occurs. Reactive oxygen species involving several pathways such as water–water cycle, Halliwell–Asada, glutathione peroxidase, Haber–Weiss and Fenton reactions helps in protecting plants against toxic radicals which otherwise could cause damage to lipophilic protein. Genetic approaches to elucidate and map genes or quantitative trait loci conferring thermotolerance will facilitate marker-assisted breeding for heat tolerance and also pave the way for characterizing genetic factors which could be useful for engineering plants with improved heat tolerance. This review discusses the protective mechanism of heat stress responses encompassing different pathways that provide tolerance during HT stress.     

植物耐热性及热激信号转导机制研究进展

随着温室效应的加剧,全球气候变暖已经成为现代农业生产体系所面临的严峻挑战．高温灾害性气候是影响作物产量的一种主要的非生物胁迫．因此,对于农作物生产而言,研究植物耐热信号转导机制不仅有重要的科学意义,而且有现实的紧迫性．最近几年,在阐明植物耐热信号转导机制的研究方面取得了很多重要的进展,这些进展涵盖植物高温胁迫的感受机制、热激转录因子和热激蛋白的表达调控、热激转录因子结合蛋白参与耐热性调控的分子机制等几个主要的方面．热胁迫影响细胞膜系统、RNA、蛋白质的稳定性,同时改变酶的活性和细胞骨架系统．当热胁迫来临时,植物的转录组会发生显著变化,所涉及的基因大约占基因组的2％．这些高温胁迫响应基因构成了热激响应网络,是植物抵御热胁迫的第一道防线．植物的耐热性分为基础耐热性和获得性耐热性．基础耐热性是植物固有的耐热性．获得性耐热性是温和的热驯化诱导的耐热性．获得性耐热性状的形成反映了植物在自然生长环境下适应高温胁迫的生理机制．     

Molecular events associated with acquisition of heat tolerance by the yeast Saccharomyces cerevisiae

Abstract: The heat shock response is an inducible protective system of all living cells. It simultaneously induces both heat shock proteins and an increased capacity for the cell to wisthstand potentially lethal temperatures (an increased thermotolerance). This has lead to the suspicion that these two phenomena must be inexorably linked. However, analysis of heat shock protein function in Saccharomyces cerevisiae by molecular genetic techniques has revealed only a minority of the heat shock proteins of this organism having appreciable influences on thermotolerance. Instead, physiological perturbations and the accumulation of trehalose with heat stress may be more important in the development of thermotolerance during a preconditioning heat shock. Vegetative S. cerevisiae also acquires thermotolerance through osmotic dehydration, through treatment with certain chemical agents and when, due to nutrient limitation, it arrests growth in the GI phase of the cell cycle. There is evidence for the activities of the cAMP-dependent protein kinase and plasma membrane ATPase being very important in thermotolerance determination. Also, intracellular water activity and trehalose probably exert a strong influence over thermotolerance through their effects on stabilisation of membranes and intracellular assemblies. Future investigations should address the unresolved issue of whether the different routes to thermotolerance induction cause a common change to the physical state of the intracellular environment, a change that may result in an increased stabilisation of cellular structures through more stable hydrogen bonding and hydrophobic interactions.