Occurrence of stem canker of tomato caused by a distinct pathotype of <I>Alternaria alternata</I> in Japan

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.

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Sphingosine-related mycotoxins in plant and animal diseases

Canadian Journal of Botany ◽

10.1139/b95-283 ◽

1995 ◽

Vol 73 (S1) ◽

pp. 459-467 ◽

Cited By ~ 33

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.

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Cultivar reactions and the genetic basis of resistance to alternaria stem canker (Alternaria alternata f.sp. lycopersici) in tomato

Plant Pathology ◽

10.1111/j.1365-3059.1988.tb02087.x ◽

1988 ◽

Vol 37 (3) ◽

pp. 373-376 ◽

Cited By ~ 3

Author(s):

D. J. VAKALOUNAKIS

Keyword(s):

Alternaria Alternata ◽

Genetic Basis ◽

Stem Canker ◽

Alternaria Stem Canker

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2001.14.4.460 ◽

2001 ◽

Vol 14 (4) ◽

pp. 460-470 ◽

Cited By ~ 24

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.

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First Report of Stem Canker Caused by Alternaria alternata on Cotton

Plant Disease ◽

10.1094/pdis.2000.84.1.103a ◽

2000 ◽

Vol 84 (1) ◽

pp. 103-103 ◽

Cited By ~ 8

Author(s):

I. A. Laidou ◽

E. K. Koulakiotu ◽

C. C. Thanassoulopoulos

Keyword(s):

Alternaria Alternata ◽

Disease Incidence ◽

Three Dimensional ◽

Morphological Characteristics ◽

Stem Canker ◽

Northern Greece ◽

First Report ◽

Stem Blight ◽

Leaf Spots ◽

Boll Rot

A stem blight of cotton (Gossypium hirsutum L.) was observed on plants of cv. 132 in the district of Ammoudia near Serres in northern Greece. Symptoms of the disease include cankers on the stem, leaf spots, and boll rots. Affected plants show early defoliation and maturing, as well as total or partial necrosis. Symptoms on stems include dark brown, circular spots that enlarge rapidly. The center of the lesions sink to form a canker. Gradually the spots become elliptical, and the tissues split the stem longitudinally, resulting in the total or partial death of the plant. The fungus isolated from infected stem tissues was identified as typical Alternaria alternata (Nees:Fr.) Keissler, based on morphological characteristics of conidia, which are produced in a loose three-dimensional tuft of branching chains (2). Pathogenicity tests were conducted by inoculating 50 cotton stems with 5-mm disks from 9-day-old cultures on potato dextrose agar at 25°C. Each stem was inoculated with three disks, and plants were placed at room temperature for 10 days for disease development. Inoculated plants exhibited more than 95% disease incidence, and frequency of reisolation was more than 70%. A. alternata is commonly known as a leaf spot, boll rot, and seedling blight pathogen of cotton. The only reported stem blight pathogen of cotton is A. macrospora (1). This is the first report of typical A. alternata as the cause of stem blight on cotton. References: (1) L. Ling and F. Y. Yang. Phytopathology 31:664, 1941. (2) E. G. Simmons. Mycotaxon 48:109, 1993.

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

Plants ◽

10.3390/plants10010047 ◽

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.

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