Heat‐induced protection against death of suspension‐cultured apple fruit cells exposed to low temperature

Wang, C. Y.; Bowen, Judith; Weir, Iona E.; Allan, Andrew C.; Ferguson, Ian B.

doi:10.1046/j.1365-3040.2001.00770.x

Cited by 38 publications

(19 citation statements)

References 42 publications

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“…One of these (ACR556) encodes the defenserelated enzyme caffeic acid 3-O-methytransferase (COMT), one of the principal enzymes in the complex network of reactions occurring as part of lignin biosynthesis and involved in the level of cell wall crosslinking in lignified tissues (Lee et al 1997). Thus, the observed changes in ACR556 transcript level may indicate that heat conditioning could have an effect on cell wall fortification, supporting the idea that a prior heating may retard chilling-induced physical changes in cell structure and function (Wang et al 2001). Other genes (ACR86 and ACR659) within group 2 were homologues to proteins involved in oxidative stress.…”

Section: Resultsmentioning

confidence: 85%

“…Chilling injury (CI) results from exposure to low, nonfreezing, temperature and eventually ends up with cell death (Wang et al 2001). Most of the knowledge about the molecular cold responses arises from studies conducted with the chilling-tolerant plant Arabidopsis thaliana (Seki et al 2001;Thomashow 2001), while research on chilling-sensitive plants has been rather scarce.…”

Section: Introductionmentioning

confidence: 99%

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A survey of genes differentially expressed during long-term heat-induced chilling tolerance in citrus fruit

Sanchez-Ballesta

Lluch

Gosalbes

et al. 2003

Planta

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Long-term storage at low, non-freezing, temperature (1.5 degrees C) induces chilling injury in fruit of Fortune mandarin (Citrus clementina Hort. Ex Tanaka x Citrus reticulata, Blanco), manifested as pitting and brown depressed areas that may end up with local cell death. Pre-conditioning of fruit for 3 days at 37 degrees C prevented chilling injury. The use of suppression subtractive hybridization permitted the isolation of genes differentially expressed in heat-conditioned fruit exposed to chilling conditions, which may be candidates for heat-induced chilling tolerance. Northern blot analysis revealed that some genes were up-regulated by prolonged heat (3 days/37 degrees C) and their expression persisted in fruit cells upon subsequent chilling exposure. The expression of other genes was specifically induced by the combination of heat and cold. Among the putative tolerance-associated genes, we identified two transcription factors of the WRKY family and one TFIIB factor. Heat conditioning also altered the expression of genes encoding proteins involved in secondary metabolism, cell wall modification, oxidative damage and other stress-responsive proteins. These results illustrate the complexity of molecular mechanisms operating during heat-induced chilling tolerance in citrus fruit.

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Section: Resultsmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

A survey of genes differentially expressed during long-term heat-induced chilling tolerance in citrus fruit

Sanchez-Ballesta

Lluch

Gosalbes

et al. 2003

Planta

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“…To establish whether AP2D7 is transcriptionally regulated by cold, apple cell cultures (Wang et al, 2001) were treated with cold (1°C) or cold followed by a 25°C treatment. Expression analysis revealed that AP2D7 was strongly regulated by cold (Fig.…”

Section: Cold Regulation Of Ap2d7/cbf2 In Cell Culturementioning

confidence: 99%

The Role of Ethylene and Cold Temperature in the Regulation of the Apple POLYGALACTURONASE1 Gene and Fruit Softening

et al. 2010

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Fruit softening in apple (Malus 3 domestica) is associated with an increase in the ripening hormone ethylene. Here, we show that in cv Royal Gala apples that have the ethylene biosynthetic gene ACC OXIDASE1 suppressed, a cold treatment preconditions the apples to soften independently of added ethylene. When a cold treatment is followed by an ethylene treatment, a more rapid softening occurs than in apples that have not had a cold treatment. Apple fruit softening has been associated with the increase in the expression of cell wall hydrolase genes. One such gene, POLYGALACTURONASE1 (PG1), increases in expression both with ethylene and following a cold treatment. Transcriptional regulation of PG1 through the ethylene pathway is likely to be through an ETHYLENE-INSENSITIVE3-like transcription factor, which increases in expression during apple fruit development and transactivates the PG1 promoter in transient assays in the presence of ethylene. A coldrelated gene that resembles a COLD BINDING FACTOR (CBF) class of gene also transactivates the PG1 promoter. The transactivation by the CBF-like gene is greatly enhanced by the addition of exogenous ethylene. These observations give a possible molecular mechanism for the cold-and ethylene-regulated control of fruit softening and suggest that either these two pathways act independently and synergistically with each other or cold enhances the ethylene response such that background levels of ethylene in the ethylene-suppressed apples is sufficient to induce fruit softening in apples.

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“…Briefly, protoplasts were suspended in PBS containing 50 lg PI ml À1 plus 0.1% Triton X-100 (v/v) and 60 lg ml À1 RNase (w/v) and the protoplasts were analyzed by the use of a flow cytometer (ESP Elite, Coulter). Cells undergoing PCD appeared in the cell cycle distribution as cells with a DNA content of less than that of G 1 cells and were estimated with Listmode software (Wang et al 2001).…”

Section: Dna Extraction and Analysismentioning

confidence: 99%

Salt stress-induced programmed cell death via Ca2+-mediated mitochondrial permeability transition in tobacco protoplasts

Lin

Wang

2005

Plant Growth Regul

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The change in cytosolic free concentration of calcium ([Ca 2+ ] cyt ) plays a key role in regulating apoptosis in animal cells. In our experiment, we tried to investigate the function of Ca 2+ in programmed cell death (PCD) in tobacco (Nicotiana tobacum, cultivar BY-2) protoplasts induced by salt stress. An obvious increase in [Ca 2+ ] cyt was observed a few minutes after treatment and the onset of a decrease in mitochondrial membrane potential (DW m ) was also observed before the appearance of PCD, pre-treatment of protoplasts with EGTA or LaCl 3 effectively retarded the increase in [Ca 2+ ] cyt , which was concomitant with the decrease in the percentage of cell death and higher DW m , pre-treatment with cyclosporine A (CsA) also effectively retarded the increase in [Ca 2+ ] cyt , the decrease in DW m and the onset of PCD. All these results suggest that Ca 2+ is a necessary element in regulating PCD and the increase in [Ca 2+ ] cyt and the opening of mitochondrial permeability transition pore (MPTP) could promote each other in regulating PCD in tobacco protoplasts induced by salt stress.Abbreviations: AIF -apoptosis inducing factor; ANT -adenine nucleotide translocator; [Ca 2+ ] cytcytosolic free calcium concentration; CsA -cyclosporin A; DCFH-DA -2,7-dichlorohydrofluoroscein diacetate; EB -ethidium bromide; HR -hypersensitive response; MPTP -mitochondrial permeability transition pore; PCD -programmed cell death; PI -propidium iodide; Rh123 -Rhodamine123; ROSreactive oxygen species; DW m -mitochondrial membrane potential

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Heat‐induced protection against death of suspension‐cultured apple fruit cells exposed to low temperature

Abstract: ABSTRACT

Cited by 38 publications

References 42 publications

A survey of genes differentially expressed during long-term heat-induced chilling tolerance in citrus fruit

A survey of genes differentially expressed during long-term heat-induced chilling tolerance in citrus fruit

The Role of Ethylene and Cold Temperature in the Regulation of the Apple POLYGALACTURONASE1 Gene and Fruit Softening

Salt stress-induced programmed cell death via Ca2+-mediated mitochondrial permeability transition in tobacco protoplasts

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