Programmed Cell Death and Postharvest Deterioration of Horticultural Produce

Programmed cell death (PCD) is a process where cells or tissues are broken down in an orderly and predictable manner, whereby nutrients are re-used by other cells, tissues or plant parts. The process of (petal) senescence shows many similarities to autophagic PCD in animal cells including a massive breakdown of protein, DNA and RNA, the formation of autophagic vacuoles for the breakdown of cytoplasm and organelles therein and, the eventual rupture of these vacuoles that kills the cell. Common storage disorders such as scald, internal browning, core breakdown and senescent breakdown in fruit and formation of a variety of storage-related problems in vegetables that are induced by severe conditions such as low temperature, low oxygen and increased carbon dioxide concentrations, are accompanied by death and sometimes disappearance of cells. This type of cell death shows similarities to autophagic cell death during aerenchyma formation in flooded roots. This paper discusses different types of cell death in relation to flower petal senescence and storage disorders in fruit and vegetables

Hypersensitive cell death in plants : its mechanisms and role in plant defense against pathogens

This review is a recent update in the understanding of the hypersensitive response (HR) of plants with special consideration to the physiological and biochemical determinants in different model systems. Hypersensitive response is reviewed as a form of programmed cell death (PCD) representing one of the mechanisms of plant defence against diseases. Major signalling pathways and molecules that accompany the HR, such as proteolytic cascades, oxidative events and ethylene that are supposed to play a key role in the plant¿s cell death machinery are discussed. Special attention is paid to the HR in fruit species. Studies on plant PCD are shown to provide a clue to better understanding disease resistance processes in plants and to establish the evolutionary aspects of PCD similarities through animal and plant kingdoms

Toxin- and cadmium-induced cell death events in tomato suspension cells resemble features of hypersensitive response

Elicitors of different origin (fumonisin B1, fungal toxin), camptothecin (alkaloid from Camptotheca acuminata), mastoparan (wasp venom) and the heavy metal (cadmium) were tested for their ability to induce programmed cell death (PCD) in a model system of tomato cell culture, line MsK8. By employing a pharmacological approach the involvement of proteolysis, oxidative stress and ethylene in the suicidal cascade is shown. The caspase-specific peptide inhibitors: irreversible caspase-1 (ICE)-inhibitor acyl-Tyr-Val-Ala-Asp-chloromethylketone and the broad range caspase inhibitor benzyoxycarbonyl-Asp-2,6-dichlorobenzoyloxymethylketone effectively reduced cell lethality providing a sound indication that in tomato suspension cells the applied inducers promote cell death that resembles features typical for PCD. A lack of inhibition occurred at mastoparan-induced cell death in response to the caspase inhibitors, while the serine protease inhibitor aminoethylbenzenesulphonyl fluoride caused substantial reduction of cell mortality. Significant inhibition was detected after administration of ethylene inhibitor, aminoethoxyvinyl glicine and the antioxidants Lgalactonic acid -¿-galactone and catalase. The results indicate that the cell death response at the exposure to biotic and abiotic stressors may employ an activation of similar cell death pathways and that caspase-like- and non-caspase-like-dependent biochemical processes may be operative. In addition, the presented comparative study suggests that the reaction of tomato suspension cells to diverse cell death stimulating compounds at least partially coincides with the cell death machinery involved in the plant hypersensitive response and during PCD in animal cells

Plant programmed cell death, ethylene and flower senescence

Programmed cell death (PCD) applies to cell death that is part of the normal life of multicellular organisms. PCD is found throughout the animal and plant kingdoms; it is an active process in which a cell suicide pathway is activated resulting in controlled disassembly of the cell. Most cases of PCD described in animal systems take the form of apoptosis, a cell death process characterised by specific features such as cell shrinkage, blebbing of the plasma membrane, condensation and fragmentation of the nucleus and internucleosomal cleavage of DNA. The final stage of apoptosis is the fragmentation of the cell into cellular debris-containing vesicles called `apoptotic bodies` that are being phagocytosed by other cells. A specific class of cell death- associated cystein proteases (caspases) has been identified. Generally, apoptotic cell death involves a sequence of caspase activation events in which initiator caspases activate down-stream executioner caspases that process a variety of target proteins eventually leading to the apoptotic phenotype. The occurrence of hallmarks of animal apoptosis was studied in tomato cells treated with the anticancer drug and inducer of apoptosis, camptothecin (cpt). It was shown that cpt-induced cell death is accompanied by nuclear condensation, the appearance of TUNEL-positive nuclei, DNA laddering and formation of DNA-containing (apoptotic) bodies and was greatly inhibited by inhibitors of animal caspases. Together the results indicate that cpt induced a cell death pathway with similarities to caspase-mediated (apoptotic) cell death in animal systems. We used cpt-treated cells to study the possible involvement of ethylene in cell death. Treatment of the cells with relatively high concentrations of ethylene did not have any effect on viability of the cells. However, when ethylene was applied in combination with cpt, a significant increase in cell death was observed as compared to cpt treatment alone. Experiments with inhibitors of ethylene production or ethylene action showed that ethylene is an essential factor mediating cpt-induced cell death. Flower senescence is accompanied by rapid death of large numbers of cells. In situ DNA degradation was studied in gypsophila petals using TUNEL. We showed that TUNEL positive nuclei appear well before the onset of the increase in ethylene production and visible signs of senescence. The role of PCD in flower senescence is discussed

Nitric oxide prevents wound-induced browning and delays senescence through inhibition of hydrogen peroxide accumulation in fresh-cut lettuce

As a source of bioactive ingredients, lettuce is a preferable component of a healthy diet. In recent years the production of fresh-cut produce has become a fast growing business. However, the shreds are highly sensitive to wound-induced browning and premature senescence that substantially reduces the visual and sensory qualities and shortens the shelf life. To improve the fresh-cut quality, in this work, short pre-storage exposure of shreds from butterhead and iceberg lettuce to nitric oxide (NO) gas was applied. It was found that fumigation with 100 and 200 ppm NO for 1 or 2 h remarkably inhibited the browning of the cut surface and of other injured leaf areas; NO treatment delayed the senescence and substantially prolonged the shelf life upon storage at 4 °C and 12 °C. To obtain information on the physiological processes involved in the wound response, the generation of hydrogen peroxide (H2O2) and the occurrence of cell death were analyzed. The results revealed that the wounding stimulated the accumulation of H2O2 thus generating oxidative stress leading to cell death. A correlation between elevated H2O2 levels, cut surface browning, senescence and storability of the fresh-cuts was established. In comparison to mature leaves, younger leaves expressed a lesser susceptibility to wound-induced browning and the associated oxidative stress. Applied NO strongly inhibited the H2O2 accumulation which may explain its beneficial effects

Chemical- and pathogen-induced programmed cell death in plants

This review focuses on recent update in the understanding of programmed cell death regarding the differences and similarities between the diverse types of cell death in animal and plant systems and describes the morphological and some biochemical determinants. The role of PCD in plant development and stress response, the involvement of plant proteases with similarities to animal caspases and the role of oxidative stress and ethylene have been discussed as key players in plant suicidal machinery. Our contribution to chemical and pathogen-induced cell death in tomato cell culture in response to camptotecin and cadmium and in response to P. syringae pv. tabaci respectively has been described and discussed. Hypersensitive response has been reviewed as a form of plant PCD representing the defence against diseases and some of the major biochemical features of HR have been discussed. The importance of studies on HR in terms of manipulation the disease resistance in plants has been outlined. Studies on plant PCD have been demonstrated to provide a clue to better understanding the process in plants and to establish the evolutionary aspects of PCD similarities through animal and plant kingdoms

Involvement of phospholipase D-related signal transduction in chemical-induced programmed cell death in tomato cell cultures

Phospholipase D (PLD) and its product phosphatidic acid (PA) are incorporated in a complex metabolic network in which the individual PLD isoforms are suggested to regulate specific developmental and stress responses, including plant programmed cell death (PCD). Despite the accumulating knowledge, the mechanisms through which PLD/PA operate during PCD are still poorly understood. In this work, the role of PLD alpha 1 in PCD and the associated caspase-like proteolysis, ethylene and hydrogen peroxide (H2O2) synthesis in tomato suspension cells was studied. Wild-type (WT) and PLD alpha 1-silenced cell lines were exposed to the cell death-inducing chemicals camptothecin (CPT), fumonisin B1 (FB1) and CdSO4. A range of caspase inhibitors effectively suppressed CPT-induced PCD in WT cells, but failed to alleviate cell death in PLD alpha 1-deficient cells. Compared to WT, in CPT-treated PLD alpha 1 mutant cells, reduced cell death and decreased production of H2O2 were observed. Application of ethylene significantly enhanced CPT-induced cell death both in WT and PLD alpha 1 mutants. Treatments with the PA derivative lyso-phosphatidic acid and mastoparan (agonist of PLD/PLC signalling downstream of G proteins) caused severe cell death. Inhibitors, specific to PLD and PLC, remarkably decreased the chemical-induced cell death. Taken together with our previous findings, the results suggest that PLD alpha 1 contributes to caspase-like-dependent cell death possibly communicated through PA, reactive oxygen species and ethylene. The dead cells expressed morphological features of PCD such as protoplast shrinkage and nucleus compaction. The presented findings reveal novel elements of PLD/PA-mediated cell death response and suggest that PLD alpha 1 is an important factor in chemical-induced PCD signal transduction