Toxins in Plant Disease
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Proposed model of signal transduction and regulatory controls for cercosporin biosynthesis and self-protection in Cercospora nicotianae. CTB8 induces the pathway. Several approaches have been used to study the importance of cercosporin in disease development 7 for the Cercospora species that synthesize this toxin. Cercosporin can be isolated from lesions on infected plants, indicating its production during infection.
Ultrastructural studies of C. Studies in several Cercospora -host systems have documented the importance of light in normal symptom development.
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For example, shading has been shown to reduce penetration of coffee leaves by C. On sugar beet, symptoms of C. Unlike the study with coffee, no reduction was noted in penetration, suggesting that colonization within the leaf is also impacted by low light conditions. Further analysis of the importance of cercosporin in disease development has been done with mutants of several species that are reduced or deficient in cercosporin biosynthesis 8. In our work, we have disrupted the gene CTB1 encoding the polyketide synthase responsible for cercosporin production in C.
Phytotoxins and their involvement in plant diseases. Introduction | SpringerLink
These mutants produce no cercosporin Fig. When inoculated onto tobacco, the ctb1 mutants produced fewer lesions and did not cause the necrotic blighting symptom characteristic of wild type infection Fig. These results demonstrate that, although not absolutely required for infection, cercosporin is a virulence factor that significantly enhances the amount and severity of disease. TLC plate showing production of cercosporin by the C.
Symptom expression on tobacco caused by the wild type C. Figures from Choquer et al. Plant-Microbe Interact.
Natural toxins in food
Given the evidence for an important role for cercosporin in disease severity, we hypothesized that defense mechanisms targeted against cercosporin may provide an additional strategy for developing resistance to these important pathogens. Due to its production of activated oxygen species, cercosporin shows almost universal toxicity to cells, with activity documented against not only plants, but also bacteria, most fungi, and mice 8. The only organisms that show high levels of resistance to cercosporin are Cercospora species and other fungi that produce perylenequinone toxins, such as Alternaria and Cladosporium.
Thus our labs and others have studied the mechanisms that Cercospora fungi use for autoresistance to cercosporin, with the goal of using fungal resistance genes as a novel source of resistance in transgenic plants. Several approaches have been used to identify genes for resistance. Upchurch and co-workers characterized genes in C.
Among the genes identified by that group was CFP described above. Not only was this gene shown to encode a transporter involved in cercosporin production, but cfp disruption mutants were also shown to be more sensitive to cercosporin than was the wild type strain. Further, expression of CFP in a cercosporin-sensitive fungus Cochliobolus heterostrophus enhanced resistance to cercosporin 20 , presumably by transporting cercosporin out of the cell.
Increased cercosporin resistance in bacteria has been identified in strains of Xanthomonas campestris pathovar zinniae that were identified by their ability to degrade cercosporin into a non-toxic compound, xanosporic acid Cercosporin degradation was shown to require a gene encoding a putative oxidoreductase. Five independent non-degrading mutants all had mutations in the oxidoreductase gene, and degradation ability was restored when the mutants were transformed to express the wild type gene.
This gene was also significantly up-regulated when the bacteria were exposed to cercosporin. Other cercosporin resistance genes have been identified through screening of C. Genes required for resistance were then identified by complementing the mutants with a library from the wild type strain. This approach identified three genes as essential for cercosporin resistance. Two of these were shown to encode enzymes in the vitamin B6 pathway and the third gene encodes a zinc cluster transcription factor. The discovery of the vitamin B6 biosynthetic genes as essential for cercosporin resistance was an interesting discovery, as this vitamin, unlike other vitamins such as vitamin E and vitamin C, had not been known to play a role in antioxidant defenses.
Vitamin B6 pyridoxal phosphate and its vitamers is an essential co-factor for enzymatic reactions, most notably transamination reactions involved in amino acid synthesis. We have subsequently shown, however, that B6 vitamers quench singlet oxygen and superoxide and have antioxidant activity 10,12 , providing an explanation for its cercosporin-protecting activity.
Finally, the CRG1 transcription factor described above was shown to affect cercosporin resistance as well as production 3. Mutants disrupted for crg1 are highly sensitive to cercosporin, along with being suppressed for production. Thus, we hypothesize that CRG1 regulates cercosporin-resistance genes. In order to identify the genes regulated by CRG1, we created a subtractive library containing sequences that are differentially regulated between the crg1 mutant and wild type.
This library contains unique sequences that are currently being characterized for a possible role in cercosporin resistance. Several studies have tested the efficacy of the microbial genes described above in providing resistance when transformed into plants. Unfortunately, thus far these studies have been met with limited or no success. The most effective approach to date has been with the cercosporin transporter, CFP. Expression of the C. Other efforts have not been as successful. The X. Extensive efforts to identify additional genes involved in cercosporin degradation through selection and complementation of non-degrading X.
We hypothesize that such mutants may be lethal, and that an alternate approach, such as searching for cercosporin-regulated genes, may allow for the identification of other genes essential for degradation and resistance.
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Considerable efforts were directed toward engineering tobacco for constitutive expression of the vitamin B6 genes, with a goal of enhancing not only cercosporin resistance, but also as a model to engineer increased abiotic stress resistance as well as improved nutritional content of crop plants. Tobacco was transformed to express the C. We co-transformed haploid tobacco with two plasmids containing the individual genes.
Transformed plants were selected in vitro for kanamycin resistance, and further screened in the greenhouse by spraying with bialaphos. Plants with resistance to both markers were put through a chromosome doubling protocol, resulting in the recovery of diploid plants homozygous for both PDX genes Fig. Haploid tobacco was co-transformed with PDX1 and PDX2 on plasmids containing selectable markers for kanamycin and bialaphos resistance, respectively. Transformed plants were selected in vitro for kanamycin resistance and further screened in the greenhouse by spraying with bialaphos.
Plants with resistance to both markers were put through a chromosome doubling protocol, resulting in the recovery of diploid plants homozygous for both PDX genes. This line was the only line that also showed increased activity of the PDX1 enzyme. Subsequent molecular analysis indicated that transformation with the fungal PDX genes resulted in down-regulation of the endogenous tobacco PDX genes, suggesting that the pathway is tightly regulated. The line with elevated B6 levels differed from the other lines in having high expression of the transgenes.
We tested seedlings of this line for resistance to cercosporin toxicity, but no differences were found, indicating that a modest increase in B6 levels is not sufficient to impart cercosporin resistance. As a comparison, C. Although other strategies may allow for increasing B6 levels in plants, our results suggested that increased B6 levels may be debilitating to plants, resulting in delayed germination and slow seedling growth.
Studies in yeast have also documented growth impairments in strains transformed to express B6 genes. Thus a strategy of increasing B6 levels may hold promise for providing cercosporin resistance, but may have unacceptable side effects for the plant. Our current efforts are focused on genes recovered from the subtractive library described above.
The role that the CFP transporter plays in cercosporin resistance was described above. In addition, studies in yeast and Botrytis have also identified ABC and MFS transporters that provided resistance to cercosporin 14, We are currently characterizing the role of our subtractive library transporters in cercosporin resistance and production using gene disruption techniques.
Cercosporin plays an important role in Cercospora pathogenicity and lesion formation in several crop species. Thus, any means of reducing cercosporin toxicity promises to have an important application for managing Cercospora leaf spot diseases in the field. In addition, cercosporin is very toxic due to the production of reactive oxygen species.
Breeding for Cercospora disease resistance has been difficult since cercosporin has general toxicity to cells. Through our studies, we found that biosynthesis and regulation of cercosporin is a complicated process. Also, the mechanisms by which the Cercospora fungi operate to protect themselves against cercosporin toxicity likely involve multiple factors. Continued research in understanding these cellular defense mechanisms and in developing strategies for blocking cercosporin production will lead to better management of Cercospora diseases in the future.
Callahan, T. CFP , the putative cercosporin transporter of Cercospora kikuchii , is required for wild type cercosporin production, resistance, and virulence on soybean. Choquer, M. The CTB1 gene encoding a fungal polyketide synthase is required for cercosporin toxin biosynthesis and fungal virulence in Cercospora nicotianae.
love.kovalev.com.ua/assets Chung, K. The CRG1 gene required for resistance to the singlet oxygen-generating cercosporin toxin in Cercospora nicotianae encodes a putative fungal transcription factor. Cercosporin-deficient mutants by plasmid tagging in the asexual fungus Cercospora nicotianae. Daub, M. Changes in tobacco cell membrane composition and structure caused by the fungal toxin, cercosporin. Plant Physiol.
The photoactivated Cercospora toxin cercosporin: Contributions to plant disease and fundamental biology. Photoactivated perylenequinone toxins in fungal pathogenesis of plants. FEMS Microbiol. Dekkers, K. The Cercospora nicotianae gene encoding dual O-methyltransferase and FAD-dependent monooxygenase domains mediates cercosporin toxin biosynthesis. Fungal Genet. In press. Denslow, S. Regulation of biosynthetic genes and antioxidant properties of vitamin B6 vitamers during plant defense responses.