Small RNAs in regulating temperature stress response in plants

Due to global climate change, temperature stress has become one of the primary causes of crop losses worldwide. Much progress has been made in unraveling the complex stress response mechanisms in plants, particularly in the identification of temperature stress responsive protein‐coding genes. Recently discovered microRNAs (miRNAs) and endogenous small‐interfering RNAs (siRN As) have also been demonstrated as important players in plant temperature stress response. Using high‐throughput sequencing, many small RNAs, especially miRNAs, have been identified to be triggered by cold or heat. Subsequently, several studies have shown an important functional role for these small RNAs in cold or heat tolerance. These findings greatly broaden our understanding of endogenous small RNAs in plant stress response control. Here, we highlight new findings regarding the roles of miRNAs and siRNAs in plant temperature stress response and acclimation. We also review the current understanding of the regulatory mechanisms of small RNAs in temperature stress response, and explore the outlook for the use of these small RNAs in molecular breeding for improvement of temperature stress tolerance in plants.     

Heat acclimation alters nitric oxide response in the splanchnic circulation

The role of nitric oxide (NO) mediated vasorelaxation in splanchnic blood flow during heat stress was studied in rats before and after heat acclimation (1 month, at 34°C). Superior mesenteric artery and portal vein blood flows were measured on-line in the conscious rats during heat stress at 40°C and 42°C before and after LNNA administration. NO mediated vasorelaxation in these vessels was studies in vitro, in response to pilocarpine, Ca ionophore and Na nitroprusside stimulation. The data suggest that NO is an integral part of the thermoregulatory splanchnic vasomotor response, and that heat acclimation enhances its regulatory importance.     

植物逆境驯化作用的生理与分子机制研究进展

植物在生长发育过程中要面对各种生物和非生物胁迫,目前对于植物应对胁迫的研究较为充分。在自然界中,各种逆境胁迫因子对植物的影响更多的是渐变的,逐渐积累的,在此过程中植物会通过驯化的方式适应这种形式的胁迫。尽管有关驯化作用提高植物耐逆性的研究有些报道,但其生理与分子机制现在还不十分清楚。本文主要介绍了植物应对病虫,冷,热,高盐4种环境因子的驯化过程的研究进展,同时总结了驯化过程的生理与分子机制,包括非激活状态的信号分子的积累以及表观遗传学修饰等。     

From molecular and cellular to integrative heat defense during exposure to chronic heat

Heat acclimation induces adaptive changes that improve the ability to cope with extreme environmental heat. Acclimatory homeostasis is manifested by an expanded dynamic thermoregulatory span (TRS), reflected in the intact organism by a lower temperature threshold (T(sh)) for heat dissipation, and delayed T(sh) for thermal injury. This principle shares common adaptive features with each of the thermoregulatory effectors. In the splanchnic circulation, e.g. the TRS of the thermally induced vasomotor response increases due to greater cardiac output distribution to the splanchnic vasculature, thereby increasing circulatory reserves and delaying thermal injury. During short-term heat acclimation (STHA), accelerated autonomic excitability plays a major role in the control of body temperature. Acclimatory homeostasis, however, is achieved only following long-term heat acclimation (LTHA), and is characterized by increased thermal effector efficiency, namely [effector organ output/autonomic signal] ratio >1. Two acclimatory responses, derived from our data on the acclimating rat model, are discussed: (1) acclimation of the cholinergic-muscarinic signaling for water secretion in the submaxillary gland; and (2) acclimatory mechanisms for increased contractile efficiency in the heart. Our data indicate that increased efficiency upon LTHA develops by reprogramming of gene expression. A reduced thyroid hormone level is responsible for some of the molecular adaptive cascades. Delayed thermal injury observed upon acclimation is due to enhanced cytoprotective mechanisms of which the inducible heat shock protein (HSP) 72 kDa plays a major role. Our data indicate that heat acclimation predisposes the HSP molecular machinery to respond faster and increases the constitutive level of the protein. STHA is the time-window during which most LTHA adaptations are switched on.     

Abiotic stress induces apoptotic-like features in tobacco that is inhibited by expression of human Bcl-2

The shared features between plant and animal programmed cell death are becoming increasingly apparent. In this study, human Bcl-2, an anti-apoptotic member of the Bcl-2 family of cell death regulators, was stably expressed in tobacco. Previously, we have shown that such plants were resistant/tolerant to several necrotrophic fungal pathogens. In this study, we show that transgenic plants are protected by several lethal abiotic stresses including heat, cold, menadione and hydrogen peroxide. Importantly, wild type tobacco, exposed to these treatments, not only died but during the death process exhibited features associated with mammalian apoptosis including DNA laddering, fragmentation, and the development of apoptotic bodies. These features were not observed in viable transgenic tobacco. Thus, abiotic stress induced cell death in plants can be accompanied by apoptotic-like features that are inhibited by expression of Bcl-2. These observations add to the growing body of evidence indicating trans-kingdom conservation of programmed cell death mechanisms.     

Effects of thermal acclimation on transcriptional responses to acute heat stress in the eurythermal fish Gillichthys mirabilis (Cooper)

The capacities of eurythermal ectotherms to withstand wide ranges of temperature are based, in part, on abilities to modulate gene expression as body temperature changes, notably genes encoding proteins of the cellular stress response. Here, using a complementary DNA microarray, we investigated the sequence in which cellular stress response-linked genes are expressed during acute heat stress, to elucidate how severity of stress affects the categories of genes changing expression. We also studied how prior acclimation history affected gene expression in response to acute heat stress. Eurythermal goby fish (Gillichthys mirabilis) were acclimated to 9 ± 0.5, 19 ± 0.5, and 28 ± 0.5°C for 1 mo. Then fish were given an acute heat ramp (4°C/h), and gill tissues were sampled every +4°C to monitor gene expression. The average onset temperature for a significant change in expression during acute stress increased by ～2°C for each ～10°C increase in acclimation temperature. For some genes, warm acclimation appeared to obviate the need for expression change until the most extreme temperatures were reached. Sequential expression of different categories of genes reflected severity of stress. Regardless of acclimation temperature, the gene encoding heat shock protein 70 (HSP70) was upregulated strongly during mild stress; the gene encoding the proteolytic protein ubiquitin (UBIQ) was upregulated at slightly higher temperatures; and a gene encoding a protein involved in cell cycle arrest and apoptosis, cyclin-dependent kinase inhibitor 1B (CDKN1B), was upregulated only under extreme stress. The tiered, stress level-related expression patterns and the effects of acclimation on induction temperature yield new insights into the fundamental mechanisms of eurythermy.     

Thermotolerance and heat acclimation may share a common mechanism in humans

Thermotolerance and heat acclimation are key adaptation processes that have been hitherto viewed as separate phenomena. Here, we provide evidence that these processes may share a common basis, as both may potentially be governed by the heat shock response. We evaluated the effects of a heat shock response-inhibitor (quercetin; 2,000 mg/day) on established markers of thermotolerance [gastrointestinal barrier permeability, plasma TNF-α, IL-6, and IL-10 concentrations, and leukocyte heat shock protein 70 (HSP70) content]. Heat acclimation reduced body temperatures, heart rate, and physiological strain during exercise/heat stress) in male subjects (n = 8) completing a 7-day heat acclimation protocol. These same subjects completed an identical protocol under placebo supplementation (placebo). Gastrointestinal barrier permeability and TNF-α were increased on the 1st day of exercise/heat stress in quercetin; no differences in these variables were reported in placebo. Exercise HSP70 responses were increased, and plasma cytokines (IL-6, IL-10) were decreased on the 7th day of heat acclimation in placebo; with concomitant reductions in exercise body temperatures, heart rate, and physiological strain. In contrast, gastrointestinal barrier permeability remained elevated, HSP70 was not increased, and IL-6, IL-10, and exercise body temperatures were not reduced on the 7th day of heat acclimation in quercetin. While exercise heart rate and physiological strain were reduced in quercetin, this occurred later in exercise than with placebo. Consistent with the concept that thermotolerance and heat acclimation are related through the heat shock response, repeated exercise/heat stress increases cytoprotective HSP70 and reduces circulating cytokines, contributing to reductions in cellular and systemic markers of heat strain. Exercising under a heat shock response-inhibitor prevents both cellular and systemic heat adaptations.     

Responses of the bed bug,Cimex lectularius,to temperature extremes and dehydration: levels of tolerance,rapid cold hardening and expression of heat shock proteins

This study of the bed bug, Cimex lectularius, examines tolerance of adult females to extremes in temperature and loss of body water. Although the supercooling point (SCP) of the bed bugs was approximately −20°C, all were killed by a direct 1 h exposure to −16°C. Thus, this species cannot tolerate freezing and is killed at temperatures well above its SCP. Neither cold acclimation at 4°C for 2 weeks nor dehydration (15% loss of water content) enhanced cold tolerance. However, bed bugs have the capacity for rapid cold hardening, i.e. a 1‐h exposure to 0°C improved their subsequent tolerance of −14 and −16°C. In response to heat stress, fewer than 20% of the bugs survived a 1‐h exposure to 46°C, and nearly all were killed at 48°C. Dehydration, heat acclimation at 30°C for 2 weeks and rapid heat hardening at 37°C for 1 h all failed to improve heat tolerance. Expression of the mRNAs encoding two heat shock proteins (Hsps), Hsp70 and Hsp90, was elevated in response to heat stress, cold stress and during dehydration and rehydration. The response of Hsp90 was more pronounced than that of Hsp70 during dehydration and rehydration. Our results define the tolerance limits for bed bugs to these commonly encountered stresses of temperature and low humidity and indicate a role for Hsps in responding to these stresses.     

Linking zebra mussel growth and survival with two cellular stress indicators during chronic temperature stress

Sessile aquatic invertebrates are at great risk for temperature stress. Changes in ambient temperature affect metabolic demands, thus altering energy budgets, and often reducing performance or survival of these species. Zebra mussels are highly invasive, yet little is known about their physiology under biologically relevant conditions, especially with regard to cellular parameters. This study examined the effect of temperature on zebra mussel physiology and investigated whether the levels of two cellular markers, HSP70 and AMPK activity, could serve as indicators of chronic thermal stress. Mussels were collected from a site in central Illinois, slowly acclimated to either 10, 20, or 30°C, and held at these temperatures for four weeks. Size, mortality, and the cellular markers were measured. Size and mortality data indicate heat stress at 30°C. Elevation in HSP70 levels confirmed this temperature elicits a stress response. Elevation in AMPK activity was not detected at 30°C, most likely indicating this temperature is beyond the scope for this marker, and therefore at or near the lethal limit. These data suggest this zebra mussel population experiences reduced performance and potential mortality in the field during summer months. Interestingly, cold acclimation resulted in a temporary elevation in AMPK activity, a result that has not been reported previously in ectotherms and is likely attributable to the metabolic demands of thermal acclimation.