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Global warming is predicted to alter temperatures thereby leading to a significant loss in crop productivity and yield. One target of global warming is plant sexual reproduction, which will be deeply threatened by high temperatures because the male gametophyte (the pollen) is particularly susceptible to heat stress. As a reaction to the latter, pollen enacts many responses that involve specific reprogramming of genetic, metabolic, and cellular activities. Most published works focus on a single episode of heat stress but less is known about the effects of heat pre-exposure (priming) on acquired thermotolerance (ATT). The purpose of this review is to gain a deeper understanding of ATT mechanisms in pollen and pollen tube, primarily from available literature. In particular, we will examine many facets (cell wall, cytoskeleton, ion fluxes, reactive oxygen species, etc.) that could be both targets of heat stress and active responses to priming.

Heat stress events are major factors limiting crop productivity. During summer days, land plants must anticipate in a timely manner upcoming mild and severe temperature. They respond by accumulating protective heat-shock proteins (HSPs), conferring acquired thermotolerance. All organisms synthetize HSPs; many of which are members of the conserved chaperones families. This review describes recent advances in plant temperature sensing, signaling, and response. We highlight the pathway from heat perception by the plasma membrane through calcium channels, such as cyclic nucleotide-gated channels, to the activation of the heat-shock transcription factors (HSFs). An unclear cellular signal activates HSFs, which act as essential regulators. In particular, the HSFA subfamily can bind heat shock elements in HSP promoters and could mediate the dissociation of bound histones, leading to HSPs transcription. Although plants can modulate their transcriptome, proteome, and metabolome to protect the cellular machinery, HSP chaperones prevent, use, and revert the formation of misfolded proteins, thereby avoiding heat-induced cell death. Remarkably, the HSP20 family is mostly tightly repressed at low temperature, suggesting that a costly mechanism can become detrimental under unnecessary conditions. Here, the role of HSP20s in response to HS and their possible deleterious expression at non-HS temperatures is discussed. [ABSTRACT FROM AUTHOR]

Abiotic and biotic stresses are often characterized by an induction of reactive electrophile species (RES) such as the jasmonate 12-oxo-phytodienoic acid (OPDA) or the structurally related phytoprostanes. Previously, RES oxylipins have been shown massively to induce heat-shock-response (HSR) genes including HSP101 chaperones. Moreover, jasmonates have been reported to play a role in basal thermotolerance. We show that representative HSR marker genes are strongly induced by RES oxylipins through the four master regulator transcription factors HSFA1a, b, d, and e essential for short-term adaptation to heat stress in Arabidopsis. When compared with Arabidopsis seedlings treated at the optimal acclimation temperature of 37 °C, the exogenous application of RES oxylipins at 20 °C induced a much weaker induction of HSP101 at both the gene and protein expression levels which, however, was not sufficient to confer short-term acquired thermotolerance. Moreover, jasmonate-deficient mutant lines displayed a wild-typelike HSR and were not compromised in acquiring thermotolerance. Hence, the OPDA- and RES oxylipin-induced HSR is not sufficient to protect seedlings from severe heat stress but may help plants to cope better with stresses associated with protein unfolding by inducing a battery of chaperones in the absence of heat. [ABSTRACT FROM AUTHOR]

The role of nitric oxide (NO) in thermotolerance acquired by heat acclimation (38°C) was investigated. Results showed that 38°C acclimation, on the one hand, obviously reduced hydrogen peroxide (HO) and MDA contents and ion leakage degree in rice leaves; however, on the other hand, it increased the survival of rice ( Oryza sativa L.) seedlings under 50°C heat stress. Application of nitric oxide donor, sodium nitroprusside (SNP), prior to 38°C acclimation dramatically increased the acquired thermotolerance. To elucidate the role of endogenous NO in acquired thermotolerance, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO, a specific NO scavenger) was used (scavengers are used to control the level of both exogenous and endogenous NO). Results showed that PTIO pretreatment resulted in the elimination of acquired thermotolerance induced by 38°C acclimation in rice seedlings. Nitric oxide (NO) release measurement indicated that there was indeed an abrupt elevation in the NO content in 40 min after 38°C acclimation, proving the involvement of NO in acquired thermotolerance inducement in rice seedling. [ABSTRACT FROM AUTHOR]

Acquired thermotolerance in plants refers to the ability to cope with lethal high temperatures following acclimatization at sublethal high temperatures. Acquired thermotolerance reflects an actual thermotolerance mechanism naturally occurring in plants and has been extensively used in thermotolerant line identification. In recent years, great progress has been achieved in the elucidation of biochemical, physiological, and molecular mechanisms of thermotolerance acquisition by using genomic approaches, including microarray analysis and mutation, knockout, and overexpression of related genes. Heat shock proteins (HSPs), such as Hsp101, BOBBER1, and Hsa32, have been shown to be important for inducement and maintenance of acquired thermotolerance. Downstream target genes and upstream regulation factors of HsfA2, including Hsa32, Apx2, small ubiquitin-like modifier proteins, FK506-binding proteins ROF1 (FKBP62) and ROF2 (FKBP65), and heat shock transcription factor binding protein, have been revealed to be involved in thermotolerance acquisition regulation. Moreover, the role of abscisic acid, ethylene, hydrogen peroxide, and salicylic acid in acquired thermotolerance has been demonstrated by molecular evidence from Arabidopsis mutants and transgenic lines. Most importantly, different molecular mechanisms of thermotolerance acquisition have been shown to underlie various acclimatization methods. Establishment of an experimental system similar to natural conditions is important for further exploration of natural thermotolerance mechanisms. [ABSTRACT FROM AUTHOR]

Background and Aims Molecular-based studies of thermotolerance have rarely been performed on wild plants, although this trait is critical for summer survival. Here, we focused on thermotolerance and expression of heat shock transcription factor A2 (HSFA2) and its putative target gene (chloroplast-localized small heat shock protein, CP-sHSP) in two allied aquatic species of the genus Potamogeton (pondweeds) that differ in survival on land. Methods The degree of thermotolerance was examined using a chlorophyll bioassay to assess heat injury in plants cultivated under non- and heat-acclimation conditions. Potamogeton HSFA2 and CP-sHSP genes were identified and their heat-induction was quantified by real-time PCR. Key Results The inhibition of chlorophyll accumulation after heat stress showed that Potamogeton malaianus had a higher basal thermotolerance and developed acquired thermotolerance, whereas Potamogeton perfoliatus was heat sensitive and unable to acquire thermotolerance. We found two duplicated HSFA2 and CP-sHSP genes in each species. These genes were induced by heat shock in P. malaianus, while one HSFA2a gene was not induced in P. perfoliatus. In non-heat-acclimated plants, transcript levels of HSFA2 and CP-sHSP were transiently elevated after heat shock. In heat-acclimated plants, transcripts were continuously induced during sublethal heat shock in P. malaianus, but not in P. perfoliatus. Instead, the minimum threshold temperature for heat induction of the CP-sHSP genes was elevated in P. perfoliatus. Conclusions Our comparative study of thermotolerance showed that heat acclimation leads to species-specific changes in heat response. The development of acquired thermotolerance is beneficial for survival at extreme temperatures. However, the loss of acquired thermotolerance and plasticity in the minimum threshold temperature of heat response may be favourable for plants growing in moderate habitats with limited daily and seasonal temperature fluctuations. [ABSTRACT FROM PUBLISHER]

Abstract: Treatment of Escherichia coli with non-lethal doses of heat or benzyl alcohol (BA) causes transient membrane fluidization and permeabilization, and induces the rapid transcription of heat-shock genes in a σ32-dependent manner. This early response is followed by a rapid adaptation (priming) of the cells to otherwise lethal elevated temperature, in strong correlation with an observed remodeling of the composition and alkyl chain unsaturation of membrane lipids. The acquisition of cellular thermotolerance in BA-primed cells is unrelated to protein denaturation and is not accompanied by the formation of major heat-shock proteins, such as GroEL and DnaK. This suggests that the rapid remodeling of membrane composition is sufficient for the short-term bacterial thermotolerance. [Copyright &y& Elsevier]