There are many Alternaria pathogens that produce host-specific toxins. Alternaria host-specific toxins are classified in three groups in terms of the primary site action. First group of toxins have in common an epoxy-decatrienoic acid structure and exert their primary effect on the plasma membrane of susceptible cells. The second group is represented by ACR(L)-toxin, which induces changes in mitochondria, including swelling, vesiculation of cristae, decrease in the electron density of the matrix, increase in the rate of NADH oxidation, and inhibition of malate oxidation. The third group consists of AM-toxin, which appears to exert an early effect on both chloroplasts and plasma membranes.
Ames and bacterial assays has demonstrated that Altertoxins I, II, III, toxins AOH and AME were mutagenic. A.N. Samokhvalov ( «A method for producing mutant strains of plant pathogen X. campesrtis». Invention certificate No 1473360 of 15.12.1988 (USSR) has found that Alternaria brassicola caused similar mutation in different strains of X. campestris affected xanthomonadin synthesis and virulence of the bacteria.
Is there any information about specific interaction between Alternaria toxins and bacterial/chloroplast or mitochondrial DNA?
I have found a nice paper : Alternariol acts as a topoisomerase poison, preferentially affecting the IIa isoform. Mol. Nutr. Food Res. 2009, 53, 441 – 451 DOI 10.1002/mnfr.200700379 441 (http://www.gzrr.de/assets/files/Publikationen/Publikationen%202009/2009-01Fehr_etal_AOH_MolNutrFoodRes.pdf)
Alternariol (AOH), a mycotoxin formed by Alternaria alternata, has been reported to possess genotoxic properties. In cell-free assays, AOH potently inhibited DNA relaxation and stimulated DNA cleavage activities of topoisomerase I, IIa and IIb. Stabilisation of covalent topoisomerase II–DNA intermediates by AOH was also detectable in cell culture, and here, the IIa isoform was preferentially targeted. AOH is thus characterised as a poison of topoisomerase I and II with a certain selectivity for the IIa isoform. Since topoisomerase poisoning and DNA strand breakage occurred within the same concentration range, poisoning of topoisomerase I and II might at least contribute to the genotoxic properties of AOH.
Schrader, T. J., et al. "Further examination of the effects of nitrosylation on Alternaria alternata mycotoxin mutagenicity in vitro." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 606.1-2 (2006): 61-71.
... To examine other targets for mutation, the metabolites Altertoxin I (ATX I), Altenuene (ALT), Alternariol (AOH), Alternariol monomethyl ether (AME), Tentoxin (TENT), Tenuazonic acid (TA) and Radicinin (RAD) were reexamined ± nitrosylation, using Ames Salmonella strain TA97, sensitive to frameshift mutations at a run of C's, as well as strains TA102 and TA104, reverted by base pair mutations at AT sites and more sensitive to oxidative damage. ... These results suggest ATX I, AME and AOH induce mutations at AT sites, possibly through oxidative damage, with nitrosylation enhancing ATX I frameshift mutagenicity at runs of C's. Nitrosylated ATX I was also directly mutagenic in mammalian test systems.
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