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Peter Nveawiah-Yoho, Jing Zhou, Marsha Palmer, Roger Sauve, Suping Zhou, Kevin J. Howe, Tara Fish, and Theodore W. Thannhauser

cochaperonins, heat-shock proteins, antioxidant enzymes, and signal transduction proteins (30%); Group 7, cellular detoxification (3%); Group 8, intracellular trafficking (3%); Group 9, protein turnover and post-translational modification (4%); and Group 10, DNA

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Yiwei Jiang, Yu Cui, Zhongyong Pei, Huifen Liu, and Shoujun Sun

shock proteins (HSPs), acting as molecular chaperones, assist in a balance of protein folding, assembly, and degradation under stress conditions. Some HSP70s are also expressed in unstressed plants, known as HSC70 (heat shock cognate), indicating that

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Konstantinos E. Vlachonasios, Dina K. Kadyrzhanova, and David R. Dilley

Heat-treatment of mature-green tomato fruit (Lycopersicon esculentum) for 48 h at 42°C has been shown to prevent chilling injury from developing after 2 or 3 weeks at 2°C. Using mRNA differential display, we recently cloned and characterized a cDNA that encodes a cytosolic class II small heat-shock protein (Le HSP17.6). The mRNA of Le HSP17.6 is up-regulated during heat shock and the level of transcription remains high during subsequent storage at chilling temperatures. We used mRNA differential display with gene-specific primers from the other small HSPs families and find that the transcription of the other small heat-shock proteins is up-regulated during heat shock and persists at elevated levels at 2°C for at least 2 weeks. When the fruits are returned to a permissive ripening temperature after the chilling period, the mRNA of the small HSPs declines slowly for 3 days. These results suggest that the persistence of the small heat-shock proteins at low temperatures may provide protection against chilling injury.

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Robert E. Paull and Nancy Jung Chen

Mesocarp softening during papaya (Carica papaya L.) ripening was impaired by heating at 42C for 30 min followed by 49C for 70 min, with areas of the flesh failing to soften. Disruption of the softening process varied with stage of ripeness and harvest date. The respiratory climacteric and ethylene production were higher and occurred 2 days sooner in the injured fruit than in the noninjured fruit that had been exposed to 49C for only 30 min. Skin degreening and internal carotenoid synthesis were unaffected by the heat treatments. Exposure of ripening fruit to either 42C for 4 hr or 38 to 42C for 1 hr followed by 3 hr at 22C resulted in the development of thermotolerance to exposure to the otherwise injurious heat treatment of 49C for 70 min. Four stainable polypeptide bands increased and seven declined in single-dimensional acrylamide gels following incubation of fruit at the nondamaging temperature of 38C for 2 hr. Three polypeptides showed marked increases when polysomal RNA was translated. These polypeptides had apparent molecular weights of 17, 18, and 70 kDa. Proteins with molecular weights of 46, 54, and 63 kDa had slight increases after heat treatment. The levels of these polypeptides peaked 2 hr after heat treatment and declined within 24 hr. The amount of these polypeptides in the unheated control varied with the batch of fruit. The concentration of three translated polypeptides, with apparent molecular weights of 26, 37, and 46 kDa, declined. Other polypeptides continued to be translated during and after holding papayas for 2 hr at 38C.

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S.M. Hum-Musser, T.E. Morelock, J.B. Murphy, and R.L. Henry

Seed germination of spinach (Spinacia oleracea L.) is partially inhibited by a high germination temperature (35 °C). Tolerance of high germination temperatures varies widely depending on the variety used. We ascertained that seed germination of these spinach varieties was thermoinhibited at 35 °C and secondary dormancy was not induced as seeds germinated when transferred to optimum germination conditions (20 °C). Treatment with 99% oxygen and 10 ppm kinetin significantly increased germination of thermoinhibited varieties at 35 °C. During heat stress, all organisms produce heat shock proteins (HSPs), which may function as molecular chaperons, are possibly required for the development of thermotolerance, and may be crucial for cell survival during heat stress. Western blotting of SDS-PAGE gels using antibodies to various heat shock proteins indicated that spinach varieties with the highest degree of thermotolerance have higher levels of HSP expression than varieties with the lowest degree of thermotolerance during germination. These results suggest that thermotolerance could be further improved, either through a breeding program or possibly by genetic engineering.

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David W. Davis and Karl J. Sauter

Attention has been given in recent literature to crop breeding for heat tolerance, but, as with certain other physiological traits, such as photosynthetic efficiency, practical gain has lagged. The question remains as to whether heat tolerance can be improved, and, if so, if it can most efficiently be improved by a holistic approach, as in breeding for yield following timely high temperature levels in the field environment, or whether the breeding for heat (and drought) tolerance components in the laboratory would be feasible. At issue is the identification and repeatability of key plant responses, such as cell membrane damage, heat shock protein formation, increased ethylene output and other responses, and the relevance, effectiveness and cost of screening for such traits. Results from our laboratory, and the work of others, will be reviewed.

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David W. Davis and Karl J. Sauter

Attention has been given in recent literature to crop breeding for heat tolerance, but, as with certain other physiological traits, such as photosynthetic efficiency, practical gain has lagged. The question remains as to whether heat tolerance can be improved, and, if so, if it can most efficiently be improved by a holistic approach, as in breeding for yield following timely high temperature levels in the field environment, or whether the breeding for heat (and drought) tolerance components in the laboratory would be feasible. At issue is the identification and repeatability of key plant responses, such as cell membrane damage, heat shock protein formation, increased ethylene output and other responses, and the relevance, effectiveness and cost of screening for such traits. Results from our laboratory, and the work of others, will be reviewed.

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Hua Zhang and Paul H. Jennings

Heat shock was applied to 32-h-old cucumber seedlings before chilling at 2.5C. Two cultivars, `Poinsett 76' and `Ashley', with different chilling tolerances, were tested. Using root growth after chilling as a measure of chilling tolerance, three heat shock regimes were found to induce chilling tolerance in both cultivars, with the most effective and uniform induction by heat shock at 40C for 3 h. `Ashley', the more chilling tolerant cultivar, exhibited a greater response to heat shock induction of chilling tolerance than `Poinsett 76'. Protein samples from roots were subjected to SDS-PAGE. Three low molecular weight heat shock proteins accumulated to a greater extent in the protein profile of heat-shocked `Ashley' roots. No such increase was found in the `Poinsett 76' roots. The induction of low molecular weight HSPs are discussed in relation to the heat-shock induction of chilling tolerance.

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Hua Zhang and Paul H. Jennings

The effects of heat shock duration and persistence on the induction of chilling tolerance in cucumber roots were studied using total root growth, electrolyte leakage, and membrane peroxidation as injury indices after chilling. Heat shock reduced the chilling induced electrolyte leakage, decreased membrane peroxidation as measured by MDA content, and resulted in a greater total root growth after chilling compared to the control. Heat shocks at 40°C, applied to 36 hr germinated seedlings for time periods from 1 to 15 hr, all resulted in an increase in chilling tolerance in a time-dependent manner. The heat shock induction of chilling tolerance is most effective when heat shock was imposed immediately before chilling, but the effect is persistent even 32 hr after heat shock when seedlings are held at 25°C before chilling. The possible mechanism of heat shock effect and its persistence will be discussed in relation to heat shock proteins and antioxidant enzyme systems.

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Robert E. Paull

There is a need to develop effective, non-damaging, non-polluting, non-carcinogenic procedures for insect disinfestation and disease control in fresh horticultural products. The loss of ethylene dibromide as a fumigant and the uncertainties of other fumigants, has meant that alternatives are needed. The most likely possibilities include irradiation, heat, cold and controlled atmospheres. Irradiation doses required for sterilization of insects cause only minor physiological changes, while controlled atmospheres appear to require longer periods of exposure than the postharvest life of most tropical fruit. The sensitivity of tropical commodities to temperatures less than 10°C makes cold treatments inappropriate for most tropical commodities. Heat treatments seem to be most promising. For papaya, the requirement is that the fruit core temperature reach 47.2°C, this can occasionally disrupt fruit ripening. The sensitivity to heat is modified by seasonal, variety and rate of heating factors. The sensitivity can be related to the heat shock response and the presence of heat shock proteins.