The molecular basis of heat stress responses in plants

Global warming impacts crop production and threatens food security.Elevated temperatures are sensed by different cell components.Temperature increases are classified as either mild warm temperatures or excessively hot temperatures,which are perceived by distinct signaling pathways in plants.Warm temperatures induce thermomorphogenesis,while high-temperature stress triggers heat acclimation and has destructive effects on plant growth and development.In this review,we systematically summarize the heat-responsive genetic networks in Arabidopsis and crop plants based on recent studies.In addition,we highlight the strategies used to improve grain yield under heat stress from a source-sink perspective.We also discuss the remaining issues regarding the characteristics of thermosensors and the urgency required to explore the basis of acclimation under multifactorial stress combination.

Dissecting the Heat Stress Response in Chlamydomonas by Pharmaceutical and RNAi Approaches Reveals Conserved and Novel Aspects

To study how conserved fundamental concepts of the heat stress response （HSR） are in photosynthetic eukaryotes, we applied pharmaceutical and antisense/amiRNA approaches to the unicellular green alga Chlamydomonas reinhardtii. The Chlamydomonas HSR appears to be triggered by the accumulation of unfolded proteins, as it was induced at ambient temperatures by feeding cells with the arginine analog canavanine. The protein kinase inhibitor staurosporine strongly retarded the HSR, demonstrating the importance of phosphorylation during activation of the HSR also in Chlamydomonas. While the removal of extracellular calcium by the application of EGTA and BAPTA inhibited the HSR in moss and higher plants, only the addition of BAPTA, but not of EGTA, retarded the HSR and impaired thermotoler- ance in Chlamydomonas. The addition of cycloheximide, an inhibitor of cytosolic protein synthesis, abolished the attenu- ation of the HSR, indicating that protein synthesis is necessary to restore proteostasis. HSP90 inhibitors induced a stress response when added at ambient conditions and retarded attenuation of the HSR at elevated temperatures. In addition, we detected a direct physical interaction between cytosolic HSP90A/HSP70A and heat shock factor 1, but surprisingly this interaction persisted after the onset of stress. Finally, the expression of antisense constructs targeting chloroplast HSP70B resulted in a delay of the cell＇s entire HSR, thus suggesting the existence of a retrograde stress signaling cascade that is desensitized in HSP7OB-antisense strains.

Mechanisms and molecular approaches for heat tolerance in rice (Oryza sativa L.) under climate change scenario

Rice, a staple cereal crop in many parts of the world, has been confronted with multiple environmental stresses including high temperature, negatively impacts the booting as well as anthesis growth stages. The situation is further complicated by the changing climatic conditions, resulting in gradual escalation of temperature as well as changing the rainfall pattern and frequency, thus raising a concern of food security worldwide. The situation can be combat by developing rice varieties with excellent genetics with improved morpho-physiological, biochemical, and molecular mechanisms, together can minimize the adverse effects of heat stress. Here, several strategies(encompassing genetic and genomic, and mechanisms involved) for mitigating the impact of high temperature on rice have been discussed. Finally, the utilization of genomic knowledge in augmenting the conventional breeding approaches have been comprehensively elaborated to develop heat tolerant germplasm.

Impact of acute heat stress on mitochondrial function, ultrastructure and cardiolipin distribution in Arabidopsis

Besides providing energy to sustain life,mitochondria also play crucial roles in stress response and programmed cell death.The mitochondrial hallmark lipid,cardiolipin(CL),is essential to the maintenance of mitochondrial structure and function.However,how mitochondria and CL are involved in stress response is not as well defined in plants as in animal and yeast cells.We previously revealed a role for CL in mitochondrial fission and in heat stress response in Arabidopsis.To further determine the involvement of mitochondria and CL in plant heat response,here we treated Arabidopsis seedlings with varied lengths of acute heat stress.These treatments resulted in decreases in mitochondrial membrane potential,disruption of mitochondrial ultrastructure,accumulation of mitochondrial reactive-oxygen species(ROS),and redistribution of CL to the outer mitochondrial membrane and to a novel type of vesicle.The level of the observed changes correlated with the severeness of the heat stress,indicating the strong relevance of these processes to stress response.Our findings provide the basis for studying mechanisms underpinning the role of mitochondria and CL in plant stress response.

Induction of Antioxidant and Heat Shock Protein Responses During Torpor in the Gray Mouse Lemur, Microcebus murinus

A natural tolerance of various environmental stresses is typically supported by various cytoprotective mechanisms that protect macromolecules and promote extended viability. Among these are antioxidant defenses that help to limit damage from reactive oxygen species and chaperones that help to minimize protein misfolding or unfolding under stress conditions. To understand the molecular mechanisms that act to protect cells during primate torpor, the present study characterizes antioxidant and heat shock protein（HSP） responses in various organs of control（aroused）and torpid gray mouse lemurs, Microcebus murinus. Protein expression of HSP70 and HSP90 a was elevated to 1.26 and 1.49 fold, respectively, in brown adipose tissue during torpor as compared with control animals, whereas HSP60 in liver of torpid animals was 1.15 fold of that in control（P 〈 0.05）. Among antioxidant enzymes, protein levels of thioredoxin 1 were elevated to 2.19 fold in white adipose tissue during torpor, whereas Cu–Zn superoxide dismutase 1 levels rose to 1.1 fold in skeletal muscle（P 〈 0.05）. Additionally, total antioxidant capacity was increased to 1.6 fold in liver during torpor（P 〈 0.05）, while remaining unchanged in the five other tissues. Overall, our data suggest that antioxidant and HSP responses are modified in a tissue-specific manner during daily torpor in gray mouse lemurs. Furthermore, our data also show that cytoprotective strategies employed during primate torpor are distinct from the strategies in rodent hibernation as reported in previous studies.