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

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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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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Efficient integrative transformation of the phytopathogenic fungus Alternaria alternata mediated by the repetitive rDNA sequences

Gene ◽

10.1016/0378-1119(90)90181-p ◽

1990 ◽

Vol 90 (2) ◽

pp. 207-214 ◽

Cited By ~ 24

Author(s):

Takashi Tsuge ◽

Syoyo Nishimura ◽

Hirokazu Kobayashi

Keyword(s):

Alternaria Alternata ◽

Phytopathogenic Fungus ◽

Rdna Sequences ◽

Integrative Transformation

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Mannitol metabolism in the phytopathogenic fungus Alternaria alternata

Fungal Genetics and Biology ◽

10.1016/j.fgb.2006.09.008 ◽

2007 ◽

Vol 44 (4) ◽

pp. 258-268 ◽

Cited By ~ 49

Author(s):

Heriberto Vélëz ◽

Norman J. Glassbrook ◽

Margaret E. Daub

Keyword(s):

Alternaria Alternata ◽

Phytopathogenic Fungus ◽

Mannitol Metabolism

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New tricycloalternarenes produced by the phytopathogenic fungus Alternaria alternata

Phytochemistry ◽

10.1016/s0031-9422(99)00275-7 ◽

1999 ◽

Vol 52 (4) ◽

pp. 593-599 ◽

Cited By ~ 28

Author(s):

Ralph-Peter Nussbaum ◽

Wolfgang Günther ◽

Stephan Heinze ◽

Bernd Liebermann

Keyword(s):

Alternaria Alternata ◽

Phytopathogenic Fungus

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Effect of humic acid on the composition of osmolytes and lipids in a melanin-containing phytopathogenic fungus Alternaria alternata

Environmental Research ◽

10.1016/j.envres.2020.110395 ◽

2020 ◽

pp. 110395

Author(s):

E.V. Fedoseeva ◽

V.M. Tereshina ◽

O.A. Danilova ◽

E.A. Ianutsevich ◽

O.S. Yakimenko ◽

...

Keyword(s):

Humic Acid ◽

Alternaria Alternata ◽

Phytopathogenic Fungus

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Mutation and treatment profiles of patients with concurrent EGFR and ALK actionable mutations (muts).

Journal of Clinical Oncology ◽

10.1200/jco.2019.37.15_suppl.3138 ◽

2019 ◽

Vol 37 (15_suppl) ◽

pp. 3138-3138

Author(s):

Jun Zhao ◽

Caixia Liu ◽

Hui Liu ◽

Yong He ◽

Liqiang Rao ◽

...

Keyword(s):

First Generation ◽

Low Frequency ◽

Resistance Mechanisms ◽

The Other ◽

Kaplan Meier ◽

Tki Resistance ◽

Treatment Naïve ◽

Alk Positive ◽

Egfr Tki ◽

Egfr Tkis

3138 Background: Actionable muts in EGFR and ALK define two molecular subtypes sensitive to EGFR-TKIs and ALK-TKIs, respectively. Although generally mutually exclusive, they did co-exist in some cases. However, when and how do they co-exist are not well understood. Methods: Pts with concurrent actionable muts in ALK and EGFR were selected from our database. Their mutation profiles and treatment histories were analyzed. PFS was estimated using Kaplan-Meier method. Results: Among 341 ALK-positive ( ALK-pos) and 3804 EGFR-positive ( EGFR-pos) pts, 9 (2.6% of ALK-pos, 0.2% of EGFR-pos) had concurrent EGFR and ALK actionable muts, including 3 EX19Indel + EML4-ALK, 2 EX19Indel + STRN-ALK, 2 L858R + L1152R, 1 L858R + EML4-ALK, and 1 G719C + S768I + STRN-ALK. All 9 pts had lung cancer. One pt with EX19Indel + EML4-ALK was treatment naïve. The other 8 pts have taken ≥ 1 EGFR-TKIs. The mPFS of these pts on first-generation EGFR-TKIs was 22 mo (95% CI: 11 - NR). Except for 1 pt who progressed on Gefitinib and subsequently on Osimertinib had a T790M+C797G, the other 7 EGFR-TKI resistance pts had no common known resistance muts. 3 pts ordered NGS tests before taking EGFR-TKIs. None of them had ALK muts at that time. Later, 1 pt (19Indel) gained an STRN-ALK after 15 mo on Osimertinib, 1 pt (L858R) gained an EML4-ALK after 5 mo on Gefitinib, and 1 pt (L858R) gained an L1152R after 10 mo on Afatinib. Therefore, ALK muts were likely developed as resistance mechanisms during EGFR-TKIs therapies in these 3 pts. Unfortunately, with no information on ALK status before EGFR-TKI therapies, we can not tell if the ALK muts were also developed during and conferred resistance to EGFR-TKI therapies in the other 5 pts. Both STRN-ALK and ALK L1152R were recorded 4 times in our database, and they concurred with EGFR actionable muts in 3 and 2 of the 4 records, respectively. Conclusions: ALK and EGFR actionable muts concurred at a relatively low frequency in our pts. In some cases, ALK muts were developed during EGFR-TKI therapies. Developed either together or sequentially, some combinations of EGFR and ALK muts, such as L858R with L1152R and EX19Indel with ALK fusion, may form more easily or may be preferable than other combinations for the development or evoluation of tumors.

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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

Phytopathology ◽

10.1094/phyto-08-12-0201-r ◽

2013 ◽

Vol 103 (7) ◽

pp. 733-740 ◽

Cited By ~ 15

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.

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Susceptibility of Various Crop and Weed Species to AAL-Toxin, a Natural Herbicide

Weed Technology ◽

10.1017/s0890037x0002306x ◽

1995 ◽

Vol 9 (1) ◽

pp. 125-130 ◽

Cited By ~ 38

Author(s):

Hamed K. Abbas ◽

T. Tanaka ◽

S. O. Duke ◽

C. D. Boyette

Keyword(s):

Alternaria Alternata ◽

Electrolyte Leakage ◽

Tomato Leaf ◽

Weed Species ◽

Canada Thistle ◽

Natural Herbicide ◽

Field Bindweed ◽

Minimal Damage ◽

Aal Toxin ◽

Susceptible Tomato

AAL-toxin, produced byAlternaria alternata, was investigated for its phytotoxic effects on 86 crop and weed species. On susceptible tomato leaf discs, AAL-toxin caused electrolyte leakage and chlorosis at 0.01 μM in 24 h. Plants tested exhibited a range of response. AAL-toxin damaged sensitive plants at 5 μM while other plants showed minimal damage at > 1000 μM. Cotton and the important weeds, Canada thistle, field bindweed, and velvetleaf were largely unaffected. Monocots tested were largely immune.

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