Sphingosine-related mycotoxins in plant and animal diseases

1995 ◽  
Vol 73 (S1) ◽  
pp. 459-467 ◽  
Author(s):  
David G. Gilchrist ◽  
Richard M. Bostock ◽  
Hong Wang
Keyword(s):  
Cell Death ◽  
Alternaria Alternata ◽  
Fusarium Moniliforme ◽  
Cellular Response ◽  
Stem Canker ◽  
Ceramide Synthase ◽  
Sucrose Transport ◽  
Aal Toxin ◽  
Aal Toxins ◽  
Alternaria Stem Canker

The AAL-toxins and fumonisins are a group of chemically related phytotoxic congeners produced by Alternaria alternata f. sp. lycopersici and Fusarium moniliforme, respectively, that also are widespread mycotoxins with important health implications. These mycotoxins, which bear a structural relationship to the sphingoid base, sphingosine, also incite maladies in animals ranging from neoplasms to renal, neural, and hepatic necrosis. A. alternata f. sp. lycopersici causes the Alternaria stem canker disease in tomatoes, while F. moniliforme causes pink ear rot of maize and is associated with post-harvest contamination of many different food staples. These toxins are potent inhibitors of ceramide synthase in plants and animals. Sphingoid bases are mediators of signal transduction leading to neoplasms and necrosis in animals. Significant inhibition of ceramide synthase in microsomal preparations of tomato occurs at 20 nM with an I50 in the range of 35–40 nM for both AAL-toxin, TA, and fumonisin, FB1. In plants, specific alterations of physiological processes associated with cellular response to these toxins appears to be required for cell death. A net decrease in sucrose influx to treated leaves occurs within 4 h of AAL-toxin treatment. Untreated leaves of toxin-resistant and -sensitive isolines of tomato show significant differences in sucrose transport capacity. Exogenous application of sucrose transport inhibitors mimicked AAL-toxin symptoms and enhanced cell death in susceptible lines of tomato. Conversely, the accumulation of the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACQ occurred in 1 h and increased rapidly during the next 6 h after exposure to AAL-toxin. ACC accumulation is followed by a burst in ethylene within 12 h. Application of specific inhibitors of ethylene synthesis or ethylene action results in a decrease in toxin-induced cell death. These toxins appear to be useful tools for defining biochemical and molecular features common to induced cell death in both plants and animals. Key words: AAL-toxins, fumonisins, mycotoxins, host-selective toxins, Alternaria stem canker, Alternaria alternata, Fusarium moniliforme.

scholarly journals Nonhost Resistance of Arabidopsis thaliana Against Alternaria alternata Involves both Pre- and Postinvasive Defenses but Is Collapsed by AAL-Toxin in the Absence of LOH2

2013 ◽  
Vol 103 (7) ◽  
pp. 733-740 ◽  
Author(s):  
Mayumi Egusa ◽  
Takuya Miwa ◽  
Hironori Kaminaka ◽  
Yoshitaka Takano ◽  
Motoichiro Kodama
Keyword(s):  
Arabidopsis Thaliana ◽  
Alternaria Alternata ◽  
Defense Mechanisms ◽  
Stem Canker ◽  
Hypersensitive Reaction ◽  
Nonhost Resistance ◽  
Necrotrophic Pathogen ◽  
Toxin Resistance ◽  
Tomato Pathotype ◽  
Aal Toxin

The tomato pathotype of Alternaria alternata causes Alternaria stem canker on tomato depending upon the production of the host-specific AAL-toxin. Host defense mechanisms to A. alternata, however, are largely unknown. Here, we elucidate some of the mechanisms of nonhost resistance to A. alternata using Arabidopsis mutants. Wild-type Arabidopsis showed either no symptoms or a hypersensitive reaction (HR) when inoculated with both strains of AAL-toxin-producing and non-producing A. alternata. Yet, when these Arabidopsis penetration (pen) mutants, pen2 and pen3, were challenged with both strains of A. alternata, fungal penetration was possible. However, further fungal development and conidiation were limited on these pen mutants by postinvasion defense with HR-like cell death. Meanwhile, only AAL-toxin-producing A. alternata could invade lag one homologue (loh)2 mutants, which have a defect in the AAL-toxin resistance gene, subsequently allowing the fungus to complete its life cycle. Thus, the nonhost resistance of Arabidopsis thaliana to A. alternata consists of multilayered defense systems that include pre-invasion resistance via PEN2 and PEN3 and postinvasion resistance. However, our study also indicates that the pathogen is able to completely overcome the multilayered nonhost resistance if the plant is sensitive to the AAL-toxin, which is an effector of the toxin-dependent necrotrophic pathogen A. alternata.

scholarly journals Overexpression of FBR 41 enhances resistance to sphinganine analog mycotoxin‐induced cell death and Alternaria stem canker in tomato

2019 ◽  
Vol 18 (1) ◽  
pp. 141-154 ◽  
Author(s):  
Zhiyong Shao ◽  
Yanting Zhao ◽  
Lihong Liu ◽  
Shanshan Chen ◽  
Chuanyou Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Stem Canker ◽  
Alternaria Stem Canker

scholarly journals Most AAL Toxin-Sensitive Nicotiana Species are Resistant to the Tomato Fungal Pathogen Alternaria alternata f. sp. lycopersici

2001 ◽  
Vol 14 (4) ◽  
pp. 460-470 ◽  
Author(s):  
Bas F. Brandwagt ◽  
Tarcies J. A. Kneppers ◽  
Gerard M. Van der Weerden ◽  
H. John J. Nijkamp ◽  
Jacques Hille
Keyword(s):  
Alternaria Alternata ◽  
Low Frequency ◽  
Stem Canker ◽  
Resistance Mechanisms ◽  
Phytopathogenic Fungus ◽  
Nicotiana Species ◽  
Mammalian Cell Lines ◽  
Nicotiana Langsdorffii ◽  
Susceptible Tomato ◽  
Aal Toxins

The phytopathogenic fungus Alternaria alternata f. sp. lycopersici produces AAL toxins required to colonize susceptible tomato (Lycopersicon esculentum) plants. AAL toxins and fumonisins of the unrelated fungus Fusarium moniliforme are sphinganine-analog mycotoxins (SAMs), which are toxic for some plant species and mammalian cell lines. Insensitivity of tomato to SAMs is determined by the Alternaria stem canker gene 1 (Asc-1), and sensitivity is associated with a mutated Asc-1. We show that SAM-sensitive species occur at a low frequency in the Nicotiana genus and that candidate Asc-1 homologs are still present in those species. In Nicotiana spp., SAM-sensitivity and insensitivity also is mediated by a single codominant locus, suggesting that SAM-sensitive genotypes are host for A. alternata f. sp. lycopersici. Nicotiana umbratica plants homozygous for SAM-sensitivity are indeed susceptible to A. alternata f. sp. lycopersici. In contrast, SAM-sensitive genotypes of Nicotiana spegazzinii, Nicotiana acuminata var. acuminata, Nicotiana bonariensis, and Nicotiana langsdorffii are resistant to A. alternata f. sp. lycopersici infection concomitant with localized cell death. Additional (nonhost) resistance mechanisms to A. alternata f. sp. lycopersici that are not based on an insensitivity to SAMs are proposed to be present in Nicotiana species.

scholarly journals Multiple Epoxide Hydrolases in Alternaria alternata f. sp. lycopersici and Their Relationship to Medium Composition and Host-Specific Toxin Production

1999 ◽  
Vol 65 (6) ◽  
pp. 2388-2395 ◽  
Author(s):  
Christophe Morisseau ◽  
Barney L. Ward ◽  
David G. Gilchrist ◽  
Bruce D. Hammock
Keyword(s):  
Molecular Mass ◽  
Alternaria Alternata ◽  
Epoxide Hydrolase ◽  
Pathogenic Fungus ◽  
Toxin Production ◽  
Medium Composition ◽  
Aal Toxin ◽  
Host Specific Toxins ◽  
Aal Toxins

ABSTRACT The production of Alternaria alternata f. sp.lycopersici host-specific toxins (AAL toxins) and epoxide hydrolase (EH) activity were studied during the growth of this plant-pathogenic fungus in stationary liquid cultures. Media containing pectin as the primary carbon source displayed peaks of EH activity at day 4 and at day 12. When pectin was replaced by glucose, there was a single peak of EH activity at day 6. Partial characterization of the EH activities suggests the presence of three biochemically distinguishable EH activities. Two of them have a molecular mass of 25 kDa and a pI of 4.9, while the other has a molecular mass of 20 kDa and a pI of 4.7. Each of the EH activities can be distinguished by substrate preference and sensitivity to inhibitors. The EH activities present at day 6 (glucose) or day 12 (pectin) are concomitant with AAL toxin production.

scholarly journals Tenuazonic Acid-Triggered Cell Death Is the Essential Prerequisite for Alternaria alternata (Fr.) Keissler to Infect Successfully Host Ageratina adenophora

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1010
Author(s):  
Jiale Shi ◽  
Min Zhang ◽  
Liwen Gao ◽  
Qian Yang ◽  
Hazem M. Kalaji ◽  
...  
Keyword(s):  
Cell Death ◽  
Alternaria Alternata ◽  
Hyphal Growth ◽  
Wild Type ◽  
Tenuazonic Acid ◽  
Pathogen Invasion ◽  
Ageratina Adenophora ◽  
Aal Toxin ◽  
Tea Production ◽  
Host Infection

The necrotrophic fungus Alternaria alternata contains different pathotypes that produce different mycotoxins. The pathotype Ageratina adenophora secretes the non-host-selective toxin tenuazonic acid (TeA), which can cause necrosis in many plants. Although TeA is thought to be a central virulence factor of the A. adenophora pathotype, the precise role of TeA in different stages of host infection by pathogens remains unclear. Here, an A. alternata wild-type and the toxin-deficient mutant ΔHP001 with a 75% reduction in TeA production were used. It was observed that wild-type pathogens could induce the reactive oxygen species (ROS) bursts in host leaves and killed photosynthetic cells before invading hyphae. The ROS interceptor catalase remarkably inhibited hyphal penetration and invasive hyphal growth and expansion in infected leaves and suppressed necrotic leaf lesion. This suggests that the production of ROS is critical for pathogen invasion and proliferation and disease symptom formation during infection. It was found that the mutant pathogens did not cause the formation of ROS and cell death in host leaves, showing an almost complete loss of disease susceptibility. In addition, the lack of TeA resulted in a significant reduction in the ability of the pathogen to penetrate invasive hyphal growth and spread. The addition of exogenous TeA, AAL-toxin, and bentazone to the mutant ΔHP001 pathogens during inoculation resulted in a significant restoration of pathogenicity by increasing the level of cell death, frequency of hyphal penetration, and extent of invasive hyphal spread. Our results suggest that cell death triggered by TeA is the essential requirement for successful colonization and disease development in host leaves during infection with A. adenophora pathogens.

scholarly journals Mutations Found in the Asc1 Gene That Confer Susceptibility to the AAL-Toxin in Ancestral Tomatoes from Peru and Mexico

Plants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 47
Author(s):  
Rin Tsuzuki ◽  
Rosa María Cabrera Pintado ◽  
Jorge Andrés Biondi Thorndike ◽  
Dina Lida Gutiérrez Reynoso ◽  
Carlos Alberto Amasifuen Guerra ◽  
...  
Keyword(s):  
Phylogenetic Tree ◽  
Solanum Lycopersicum ◽  
Alternaria Alternata ◽  
Stem Canker ◽  
Pathogenic Factor ◽  
Canker Disease ◽  
Nucleotide Deletion ◽  
History Of ◽  
Aal Toxin

Tomato susceptibility/resistance to stem canker disease caused by Alternaria alternata f. sp. lycopersici and its pathogenic factor AAL-toxin is determined by the presence of the Asc1 gene. Several cultivars of commercial tomato (Solanum lycopersicum var. lycopersicum, SLL) are reported to have a mutation in Asc1, resulting in their susceptibility to AAL-toxin. We evaluated 119 ancestral tomato accessions including S. pimpinellifolium (SP), S. lycopersicum var. cerasiforme (SLC) and S. lycopersicum var. lycopersicum “jitomate criollo” (SLJ) for AAL-toxin susceptibility. Three accessions, SP PER018805, SLC PER018894, and SLJ M5-3, were susceptible to AAL-toxin. SLC PER018894 and SLJ M5-3 had a two-nucleotide deletion (nt 854_855del) in Asc1 identical to that found in SLL cv. Aichi-first. Another mutation (nt 931_932insT) that may confer AAL-toxin susceptibility was identified in SP PER018805. In the phylogenetic tree based on the 18 COSII sequences, a clade (S3) is composed of SP, including the AAL-toxin susceptible PER018805, and SLC. AAL-toxin susceptible SLC PER018894 and SLJ M5-3 were in Clade S2 with SLL cultivars. As SLC is thought to be the ancestor of SLL, and SLJ is an intermediate tomato between SLC and SLL, Asc1s with/without the mutation seem to have been inherited throughout the history of tomato domestication and breeding.

scholarly journals Horizontal Chromosome Transfer, a Mechanism for the Evolution and Differentiation of a Plant-Pathogenic Fungus

2009 ◽  
Vol 8 (11) ◽  
pp. 1732-1738 ◽  
Author(s):  
Yasunori Akagi ◽  
Hajime Akamatsu ◽  
Hiroshi Otani ◽  
Motoichiro Kodama
Keyword(s):  
Fragment Length Polymorphism ◽  
Pathogenic Fungus ◽  
Stem Canker ◽  
Hybrid Strain ◽  
Dispensable Chromosome ◽  
Tomato Pathotype ◽  
Aal Toxin ◽  
Cdc Genes ◽  
Restriction Fragment Length ◽  
Alternaria Stem Canker

ABSTRACT The tomato pathotype of Alternaria alternata produces host-specific AAL toxin and causes Alternaria stem canker on tomato. A polyketide synthetase (PKS) gene, ALT1, which is involved in AAL toxin biosynthesis, resides on a 1.0-Mb conditionally dispensable chromosome (CDC) found only in the pathogenic and AAL toxin-producing strains. Genomic sequences of ALT1 and another PKS gene, both of which reside on the CDC in the tomato pathotype strains, were compared to those of tomato pathotype strains collected worldwide. This revealed that the sequences of both CDC genes were identical among five A. alternata tomato pathotype strains having different geographical origins. On the other hand, the sequences of other genes located on chromosomes other than the CDC are not identical in each strain, indicating that the origin of the CDC might be different from that of other chromosomes in the tomato pathotype. Telomere fingerprinting and restriction fragment length polymorphism analyses of the A. alternata strains also indicated that the CDCs in the tomato pathotype strains were identical, although the genetic backgrounds of the strains differed. A hybrid strain between two different pathotypes was shown to harbor the CDCs derived from both parental strains with an expanded range of pathogenicity, indicating that CDCs can be transmitted from one strain to another and stably maintained in the new genome. We propose a hypothesis whereby the ability to produce AAL toxin and to infect a plant could potentially be distributed among A. alternata strains by horizontal transfer of an entire pathogenicity chromosome. This could provide a possible mechanism by which new pathogens arise in nature.

scholarly journals Overexpression of the Tomato Asc-1 Gene Mediates High Insensitivity to AAL Toxins and Fumonisin B1 in Tomato Hairy Roots and Confers Resistance to Alternaria alternata f. sp. lycopersici in Nicotiana umbratica Plants

2002 ◽  
Vol 15 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Bas F. Brandwagt ◽  
Tarcies J. A. Kneppers ◽  
H. John J. Nijkamp ◽  
Jacques Hille
Keyword(s):  
Hairy Roots ◽  
Alternaria Alternata ◽  
Fumonisin B1 ◽  
Sphingoid Base ◽  
Plant Infection ◽  
Aal Toxin ◽  
In Vitro Treatment ◽  
Aal Toxins ◽  
Complex Sphingolipids

The sphinganine-analog mycotoxins (SAMs) fumonisin B1 and AAL toxins are inhibitors of eukaryotic sphinganine N-acyltransferase in vitro. Treatment of eukaryotes with SAMs generally results in an accumulation of sphingoid base precursors and a depletion of complex sphingolipids. The asc,asc genotypes of tomato (Lycopersicon esculentum) and Nicotiana umbratica are sensitive to SAMs and host of the AAL toxin-producing fungus Alternaria alternata f. sp. lycopersici. Codominant insensitivity to SAMs in tomato is mediated by the Asc-1 gene, and sensitivity is associated with a frame-shift mutation present in asc-1. We investigated the function of Asc-1 in mediating insensitivity to SAMs and resistance to the fungus by overexpression of asc-1 and Asc-1. In this study, it is shown that overexpression of these genes did not lead to visual symptoms in tomato hairy roots and N. umbratica plants. Overexpression of asc-1 did not influence the (in)sensitivity to SAMs. Overexpression of Asc-1 in SAM-sensitive hairy roots and N. umbratica plants, however, mediated a high insensitivity to SAMs and resistance to plant infection by Alternaria alternata f. sp. lycopersici.

Pathogenicity of Alternaria alternata and Fusarium moniliforme and Phytotoxicity of AAL-toxin and Fumonisin B1on Tomato Cultivars

1995 ◽  
Vol 143 (6) ◽  
pp. 329-334 ◽  
Author(s):  
H. K. Abbas ◽  
T. Tanaka ◽  
S. O. Duke
Keyword(s):  
Alternaria Alternata ◽  
Fusarium Moniliforme ◽  
Aal Toxin ◽  
Tomato Cultivars
Sign in / Sign up

Export Citation Format

Share Document