Molecular and genetic characterization of ethylene involvement in mycotoxin-induced plant cell death

Moore, Thomas; Martineau, Belinda; Bostock, Richard M.; Lincoln, James E.; Gilchrist, David G.

doi:10.1006/pmpp.1998.0190

Cited by 43 publications

(45 citation statements)

References 31 publications

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“…Involvement of ET in FB1-induced cell death is further supported by the observation that the ET action inhibitor Ag ϩ suppresses FB1-mediated cell death in protoplasts (T. Asai and F. Ausubel, unpublished data) and that FB1 induces the ET-forming enzyme 1-aminocyclopropane-1-carboxylic acid (ACC) oxidase (Table 1). Finally, induction of ET and its biosynthetic genes by AAL toxin and FB1 has been reported in tomato leaflets (Moussatos et al, 1994;Moore et al, 1999). ET has been well documented to be involved in developmentally controlled PCD such as senescence (Pennell and Lamb, 1997;Gray and Johal, 1998;Johnson and Ecker, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…AAL toxin is secreted by the tomato pathogen Alternaria alternata f sp lycopersici , and the structurally related toxin FB1 is produced by the maize pathogen Fusarium moniliforme . Gilchrist and co-workers have shown that these toxins induce apoptosislike cell death in tomato leaflets and protoplasts and that the cell death in the leaflets induced by AAL toxin is suppressed by inhibitors of ET biosynthesis or its action (Moussatos et al, 1994; Wang et al, 1996;Moore et al, 1999). They have further demonstrated that leaflets of the tomato never ripe mutant, which is deficient in ET perception, display fewer lesions in response to these toxins (Moore et al, 1999).…”

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confidence: 99%

“…Gilchrist and co-workers have shown that these toxins induce apoptosislike cell death in tomato leaflets and protoplasts and that the cell death in the leaflets induced by AAL toxin is suppressed by inhibitors of ET biosynthesis or its action (Moussatos et al, 1994; Wang et al, 1996;Moore et al, 1999). They have further demonstrated that leaflets of the tomato never ripe mutant, which is deficient in ET perception, display fewer lesions in response to these toxins (Moore et al, 1999). These results indicate that an ET-dependent pathway is involved in the tomato cell death signaling triggered by AAL toxin or FB1.…”

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Fumonisin B1–Induced Cell Death in Arabidopsis Protoplasts Requires Jasmonate-, Ethylene-, and Salicylate-Dependent Signaling Pathways

et al. 2000

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We have established an Arabidopsis protoplast model system to study plant cell death signaling. The fungal toxin fumonisin B1 (FB1) induces apoptosis-like programmed cell death (PCD) in wild-type protoplasts. FB1, however, only marginally affects the viability of protoplasts isolated from transgenic NahG plants, in which salicylic acid (SA) is metabolically degraded; from pad4-1 mutant plants, in which an SA amplification mechanism is thought to be impaired; or from jar1-1 or etr1-1 mutant plants, which are insensitive to jasmonate (JA) or ethylene (ET), respectively. FB1 susceptibility of wild-type protoplasts decreases in the dark, as does the cellular content of phenylalanine ammonia-lyase, a light-inducible enzyme involved in SA biosynthesis. Interestingly, however, FB1-induced PCD does not require the SA signal transmitter NPR1, given that npr1-1 protoplasts display wild-type FB1 susceptibility. Arabidopsis cpr1-1 , cpr6-1 , and acd2-2 protoplasts, in which the SA signaling pathway is constitutively activated, exhibit increased susceptibility to FB1. The cpr6-1 and acd2-2 mutants also constitutively express the JA and ET signaling pathways, but only the acd2-2 protoplasts undergo PCD in the absence of FB1. These results demonstrate that FB1 killing of Arabidopsis is light dependent and requires SA-, JA-, and ET-mediated signaling pathways as well as one or more unidentified factors activated by FB1 and the acd2-2 mutation. INTRODUCTIONPlant cell death is often the consequence of plant-pathogen interactions in both compatible and incompatible relationships (Greenberg, 1997). A notable example is localized cell collapse, called the hypersensitive response (HR), which is induced rapidly in a resistant plant at the infection site of an avirulent pathogen (Staskawicz et al., 1995; Bent, 1996; Dangl et al., 1996; Hammond-Kosack and Jones, 1996). Hypersensitive cell death, which is distinct from necrosis caused by metabolic toxins or severe trauma, is genetically programmed (programmed cell death [PCD]) and requires active host cell metabolism Morel and Dangl, 1997;Pennell and Lamb, 1997; Gilchrist, 1998; Gray and Johal, 1998; Heath, 1998;Richberg et al., 1998). In fact, plant cells undergoing the HR display several molecular and morphological markers characteristic of animal apoptosis (a specialized form of PCD), including systematic DNA degradation and formation of apoptotic-like bodies, which suggests that the terminal steps in PCD are well conserved in animals and plants (Levine et al., 1996;Ryerson and Heath, 1996; Wang et al., 1996). It remains to be determined, however, whether the signal transduction mechanisms leading to the onset of PCD are also equally conserved between the two kingdoms.Salicylic acid (SA) is the best-characterized signaling molecule in plant defense responses (Ryals et al., 1996; Delaney, 1997; Durner et al., 1997). Application of exogenous SA or SA analogs activates the expression of a variety of pathogenesis-related ( PR ) genes and enhances resistance to a variety of pathogens (W...

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Fumonisin B1–Induced Cell Death in Arabidopsis Protoplasts Requires Jasmonate-, Ethylene-, and Salicylate-Dependent Signaling Pathways

et al. 2000

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“…The burst in the oxidative metabolism generated within minutes of infection leads to the accumulation of the reactive oxygen intermediates (ROI) such as H 2 O 2 and superoxide anion (O 2 d 2 ), involving NADPH-dependent oxidase. ROI serve as signaling molecules, for example in the recognition of the attack by fungal pathogens (Lamb and Dixon, 1997).Ethylene is widely known to modulate the organ senescence induced by various stress factors such as plant pathogens (Moore et al, 2000), O 3 2 (Pell et al, 1997), and hypoxia (He et al, 1996). O 3 2 induces genes involved in the ethylene biosynthesis (Overmyer et al, 2000).…”

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“…Ethylene is widely known to modulate the organ senescence induced by various stress factors such as plant pathogens (Moore et al, 2000), O 3 2 (Pell et al, 1997), and hypoxia (He et al, 1996). O 3 2 induces genes involved in the ethylene biosynthesis (Overmyer et al, 2000).…”

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Capsicum annuumTobacco Mosaic Virus-Induced Clone 1 Expression Perturbation Alters the Plant's Response to Ethylene and Interferes with the Redox Homeostasis

Shin

Park

et al. 2004

Plant Physiology

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Capsicum annuum tobacco mosaic virus (TMV)-induced clone 1 (CaTin1) gene was expressed early during incompatible interaction of hot pepper (Caspsicum annuum) plants with TMV and Xanthomonas campestris. RNA-blot analysis showed that CaTin1 gene was expressed only in roots in untreated plants and induced mainly in leaf in response to ethylene, NaCl, and methyl viologen but not by salicylic acid and methyl jasmonate. The ethylene dependence of CaTin1 induction upon TMV inoculation was demonstrated by the decrease of CaTin1 expression in response to several inhibitors of ethylene biosynthesis or its action. Transgenic tobacco (Nicotiana tabacum) plants expressing CaTin1 gene in sense-or antisense-orientation showed interesting characteristics such as the accelerated growth and the enhanced resistance to biotic as well as abiotic stresses. Such characteristics appear to be caused by the elevated level of ethylene and H 2 O 2 . Moreover, in transgenic plants expressing antisense CaTin1 gene, the expression of some pathogenesis-related genes was enhanced constitutively, which may be mainly due to the increased ethylene level. The promoter of CaTin1 has four GCC-boxes, two AT-rich regions, and an elicitor-inducible W-box. The induction of the promoter activity by ethylene depends on GCC-boxes and by TMV on W-box. Taken together, we propose that the CaTin1 up-regulation or down-regulation interferes with the redox balance of plants leading to the altered response to ethylene and biotic as well as abiotic stresses.Multiple preformed antimicrobial compounds contribute to the constitutive defense machinery of plants against pathogenic organisms. In addition, plants can trigger the inducible defense programs upon the perception of invaders. The early signaling molecules leading to R-gene-mediated resistance are ion fluxes, GTP-binding proteins, protein kinases, phosphatases, and phospholipases (Hammond-Kosack and Jones, 1996). Plants also respond to external stimuli such as microbial elicitors of cell death and/or defense responses by changing the calcium influx of the cell (Ebel and Scheel, 1997;Higgins et al., 1998). The increase of cytosolic calcium leads to cell death, which seems necessary for hypersensitive cell death triggered by rust fungi (Xu and Heath, 1998). The calcium channel blocker La 31 , on the other hand, prevents the bacteriainduced hypersensitive response (HR) in soybean (Glycine max) leaves (Levine et al., 1996). The burst in the oxidative metabolism generated within minutes of infection leads to the accumulation of the reactive oxygen intermediates (ROI) such as H 2 O 2 and superoxide anion (O 2 d 2 ), involving NADPH-dependent oxidase. ROI serve as signaling molecules, for example in the recognition of the attack by fungal pathogens (Lamb and Dixon, 1997).Ethylene is widely known to modulate the organ senescence induced by various stress factors such as plant pathogens (Moore et al., 2000), O 3 2 (Pell et al., 1997), and hypoxia (He et al., 1996). O 3 2 induces genes involved in the ethylene biosynthes...

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Multiple mediators of plant programmed cell death: Interplay of conserved cell death mechanisms and plant‐specific regulators

2002

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Programmed cell death (PCD) is a process aimed at the removal of redundant, misplaced, or damaged cells and it is essential to the development and maintenance of multicellular organisms. In contrast to the relatively well-described cell death pathway in animals, often referred to as apoptosis, mechanisms and regulation of plant PCD are still ill-defined. Several morphological and biochemical similarities between apoptosis and plant PCD have been described, including DNA laddering, caspase-like proteolytic activity, and cytochrome c release from mitochondria. Reactive oxygen species (ROS) have emerged as important signals in the activation of plant PCD. In addition, several plant hormones may exert their respective effects on plant PCD through the regulation of ROS accumulation. The possible plant PCD regulators discussed in this review are integrated in a model that combines plant-specific regulators with mechanisms functionally conserved between animals and plants.

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Molecular and genetic characterization of ethylene involvement in mycotoxin-induced plant cell death

Cited by 43 publications

References 31 publications

Fumonisin B1–Induced Cell Death in Arabidopsis Protoplasts Requires Jasmonate-, Ethylene-, and Salicylate-Dependent Signaling Pathways

Fumonisin B1–Induced Cell Death in Arabidopsis Protoplasts Requires Jasmonate-, Ethylene-, and Salicylate-Dependent Signaling Pathways

Capsicum annuumTobacco Mosaic Virus-Induced Clone 1 Expression Perturbation Alters the Plant's Response to Ethylene and Interferes with the Redox Homeostasis

Multiple mediators of plant programmed cell death: Interplay of conserved cell death mechanisms and plant‐specific regulators

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