Fumonisins and Alternaria alternata lycopersici toxins: sphinganine analog mycotoxins induce apoptosis in monkey kidney cells.

Wang, W; Jones, Clinton; Zanella, J. R. C.; Holt, Todd; Gilchrist, David G.; Dickman, Martin B.

doi:10.1073/pnas.93.8.3461

Cited by 177 publications

(100 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It can lead to either necrosis disease (Wang et al, 1996a;Navarre and Wolpert, 1999) or disease resistance, such as extreme resistance or systemic acquired resistance (Greenberg et al, 1994; SatRNA-Induced PCD in Tomato 1083 Bendahmane et al, 1999). Disease resistance usually results from a response to incompatible pathogens.…”

Section: Pcd Is Involved In the D4-satrna-induced Systemic Necrosis Imentioning

confidence: 99%

“…The HR may result from a PCD pathway that is induced by the specific interaction between pathogen avirulence gene products and host resistance gene products, but the recognition of pathogens and the activation of the PCD pathway are poorly understood. Alternaria tomato canker disease results from the A. a. lycopersici toxin, which can also induce apoptosis in monkey kidney cells, but the molecular mechanism in tomato has not been determined (Wang et al, 1996a). The oat blight disease induced by the toxin victorin involves the specific cleavage of ribulose-1,5-bisphosphate carboxylase/oxygenase and may interact with senescence mechanisms (Navarre and Wolpert, 1999).…”

Section: Pcd Is Involved In the D4-satrna-induced Systemic Necrosis Imentioning

confidence: 99%

“…However, cell death is not well understood in most cases. In Alternaria stem canker disease of tomato caused by the toxin of the fungus ( Alternaria alternata f sp lycopersici ), cell death in the toxin-treated protoplasts and leaflets has the morphological characteristics of apoptosis (Wang et al, 1996a). In victoria blight of oats, cell death induced by victorin also has some apoptotic features (Navarre and Wolpert, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…Studies show that the HR is uncoupled from the resistance mechanism in at least some cases, indicating that the host responses of cell death and resistance may use different pathways (del Pozo and Lam, 1998;Yu et al, 1998;Bendahmane et al, 1999). PCD is involved in some cases of both pathogen-induced resistance and disease cell death (Greenberg et al, 1994;Ryerson and Heath, 1996;Wang et al, 1996aWang et al, , 1996bKosslak et al, 1997;Navarre and Wolpert, 1999). Here, cell death occurring during the systemic necrosis induced by D4-satRNA shares cellular features similar to those of PCD.…”

mentioning

confidence: 96%

“…Alternaria tomato canker disease results from the A. a. lycopersici toxin, which can also induce apoptosis in monkey kidney cells, but the molecular mechanism in tomato has not been determined (Wang et al, 1996a). The oat blight disease induced by the toxin victorin involves the specific cleavage of ribulose-1,5-bisphosphate carboxylase/oxygenase and may interact with senescence mechanisms (Navarre and Wolpert, 1999).…”

mentioning

confidence: 99%

See 4 more Smart Citations

Cucumber Mosaic Virus D Satellite RNA-Induced Programmed Cell Death in Tomato

Xu¹,

Roossinck²

2000

The Plant Cell

View full text Add to dashboard Cite

D satellite RNA (satRNA) with its helper virus, namely, cucumber mosaic virus, causes systemic necrosis in tomato. The infected plant exhibits a distinct spatial and temporal cell death pattern. The distinct features of chromatin condensation and nuclear DNA fragmentation indicate that programmed cell death is involved. In addition, satRNA localization and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling show that cell death is initiated from the infected phloem or cambium cells and spreads to other nearby infected cells. Timing of the onset of necrosis after inoculation implicates the involvement of cell developmental processes in initiating tomato cell death. Analysis of the accumulation of minus-and plus-strand satRNAs in the infected plants indicates a correlation between high amounts of minus-strand satRNA and tomato cell death. INTRODUCTIONCucumber mosaic virus (CMV) is an isometric plant virus with a tripartite plus-sense RNA genome (Palukaitis et al., 1992). Some strains of CMV harbor satellite RNAs (satRNAs)-small, linear molecules ranging from 332 to 405 nucleotides long. The satRNAs are dependent on CMV for their replication, encapsidation, and dispersion, but they are not necessary for the life cycle of the virus. They can attenuate or exacerbate the symptoms induced by the helper viruses in specific plant hosts. For example, D-satRNA, B-satRNA, and WL1-satRNA induce necrosis, chlorosis, and attenuation, respectively, in infected tomato plants in the presence of any CMV helper virus. In tobacco, however, D-satRNA and WL1-satRNA attenuate symptoms, whereas minor nucleotide sequence variants of the B-satRNA either attenuate symptoms or induce chlorosis in a helper virusspecific manner (reviewed in García-Arenal and Palukaitis, 1999).D-satRNA (335 nucleotides long) induces a lethal systemic necrosis in tomato that has been reported as epidemic in France, Italy, and Spain (Kaper and Waterworth, 1977;Jordá et al., 1992). The molecular and cellular mechanisms of the disease, which can cause a catastrophic reduction in tomato production, remain unknown, although the sequences in D-satRNA responsible for the lethal necrosis have been determined (Sleat and Palukaitis, 1990;Sleat et al., 1994). By using in vitro and in vivo analyses of its secondary structure, researchers have correlated a helix and a tetraloop region near the 3 Ј end of the satRNA with the necrotic syndrome (Bernal and García-Arenal, 1997;Rodríguez-Alvarado and Roossinck, 1997). For some specific CMV and satRNA combinations, RNA 2 of CMV has been shown to be involved in determining pathogenicity (Sleat et al., 1994). Recently, however, the minus-strand D-satRNA expressed from a potato virus X vector was shown to induce similar necrosis in tomato, thereby excluding the specific role of CMV in the pathogenicity of D-satRNA, except for its function as a helper virus in the host plants (Taliansky et al., 1998).The conspicuous symptom of tomato plants infected by D-satRNA and CMV is cell death, the cause of the lethal systemic...

show abstract

Section: Pcd Is Involved In the D4-satrna-induced Systemic Necrosis Imentioning

confidence: 99%

Section: Pcd Is Involved In the D4-satrna-induced Systemic Necrosis Imentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 96%

mentioning

confidence: 99%

See 3 more Smart Citations

Cucumber Mosaic Virus D Satellite RNA-Induced Programmed Cell Death in Tomato

Xu¹,

Roossinck²

2000

The Plant Cell

View full text Add to dashboard Cite

show abstract

Early fumonisin B1 toxicity in relation to disrupted sphingolipid metabolism in male BALB/c mice

Tsunoda

Sharma

Riley

1998

J. Biochem. Mol. Toxicol.

View full text Add to dashboard Cite

Fumonisin B1 is a mycotoxin produced by Fusarium moniliforme, a common fungus in corn. It is known to cause a variety of diseases, including hepatic and renal degeneration in many species of laboratory and domestic animals. The known biochemical events in fumonisin B1 toxicity involve inhibition of ceramide synthase leading to disruption of sphingolipid metabolism. The effect of fumonisin B1 on ceramide and more complex sphingolipids in mice is not known. Groups of five male BALB/c mice each were injected with fumonisin B1 subcutaneously at doses of 0, 0.25, 0.75, 2.25, and 6.75 mg/kg body weight daily for 5 days. This protocol has been shown to produce a dose‐dependent increase in apoptosis in liver and kidney of these animals. In the present study, liver, kidney, and brain were sampled and analyzed for free sphingoid bases and complex sphingolipids one day after the last treatment. A dose‐related accumulation of free sphinganine and sphingosine was observed in liver and kidney, but not brain. The maximal increase in free sphinganine in kidney was 10‐fold greater than in liver. Total phospholipids increased only in liver, whereas ceramide levels were not consistently altered in liver, kidney, or brain. In liver and kidney, fumonisin B1 treatment increased the sphinganine‐containing complex sphingolipids, but no effect was observed on sphingosine‐containing complex sphingolipids. No changes in complex sphingolipids were observed in brain. In liver, there was a close correlation between the extent of free sphinganine accumulation, and apoptosis and hepatopathy. This correlation was also evident in kidney but to a lessor extent. Nonetheless, the apoptosis and nephropathy occurred with little or no change in the levels of ceramide or more complex sphingolipids. © 1998 John Wiley & Sons, Inc. J Biochem Toxicol 12: 281–289, 1998

show abstract

Biological detoxification of fungal toxins and its use in plant breeding, feed and food production

1999

View full text Add to dashboard Cite

Fumonisins and Alternaria alternata lycopersici toxins: sphinganine analog mycotoxins induce apoptosis in monkey kidney cells.

Abstract: Fusarium moniliforme toxins (fumonisins) and Alternaria alternata lycopersici (AAL)

Cited by 177 publications

References 30 publications

Cucumber Mosaic Virus D Satellite RNA-Induced Programmed Cell Death in Tomato

Cucumber Mosaic Virus D Satellite RNA-Induced Programmed Cell Death in Tomato

Early fumonisin B1 toxicity in relation to disrupted sphingolipid metabolism in male BALB/c mice

Biological detoxification of fungal toxins and its use in plant breeding, feed and food production

Contact Info

Product

Resources

About