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

1988 ◽  
Vol 37 (3) ◽  
pp. 373-376 ◽  
Author(s):  
D. J. VAKALOUNAKIS
1995 ◽  
Vol 73 (S1) ◽  
pp. 459-467 ◽  
Author(s):  
David G. Gilchrist ◽  
Richard M. Bostock ◽  
Hong Wang

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.


2013 ◽  
Vol 103 (7) ◽  
pp. 733-740 ◽  
Author(s):  
Mayumi Egusa ◽  
Takuya Miwa ◽  
Hironori Kaminaka ◽  
Yoshitaka Takano ◽  
Motoichiro Kodama

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.


Plant Science ◽  
1992 ◽  
Vol 81 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Hanneke M.A. Witsenboer ◽  
Karen M. Kloosterziel ◽  
Guus Hateboer ◽  
H.John J. Nijkamp ◽  
Jacques Hille

2019 ◽  
Vol 54 (9) ◽  
pp. 781-790
Author(s):  
Elisa Zorzi Tomazoni ◽  
Rute T. S. Ribeiro ◽  
Gabriel F. Pauletti ◽  
Geraldo L. G. Soares ◽  
Joséli Schwambach

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

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

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.


1984 ◽  
Vol 26 (0) ◽  
pp. 29-32
Author(s):  
Yukio TAGAMI ◽  
Akira TOMIKAWA ◽  
Toshio YAMAMOTO ◽  
Naoe KATAGIRI ◽  
Keisuke KOHMOTO ◽  
...  

1989 ◽  
Vol 78 (4) ◽  
pp. 457-462 ◽  
Author(s):  
H. M. A. Witsenboer ◽  
E. G. van de Griend ◽  
J. B. Tiersma ◽  
H. J. J. Nijkamp ◽  
J. Hille

1993 ◽  
Vol 240 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Bert Overduin ◽  
Saskia A. Hogenhout ◽  
Erik A. van der Biezen ◽  
Michel A. Haring ◽  
H. John J. Nijkamp ◽  
...  

Plant Disease ◽  
2000 ◽  
Vol 84 (1) ◽  
pp. 103-103 ◽  
Author(s):  
I. A. Laidou ◽  
E. K. Koulakiotu ◽  
C. C. Thanassoulopoulos

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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