The novel weapons hypothesis states that some invasive weed species owe part of their success as invaders to allelopathy mediated by allelochemicals that are new to the native species. Presumably, no resistance has evolved among the native species to this new allelochemical (i.e., the novel weapon). In their native habitat, however, the plants that co-evolved with these invasive species have theoretically evolved defenses that obviate the allelochemical advantage. Previous studies have claimed that catechin is such a novel weapon of spotted knapweed (Centaurea stoebe = C. maculosa), an invasive species in the non-native habitat of North America. These studies indicated that (-)-catechin is more phytotoxic than (+)-catechin. Other studies have not found sufficient catechin in field soils to support this theory. We report that (-)-catechin and (+)-catechin are essentially equal, but poorly phytotoxic to a variety of plant species in bioassays without soil. In a dose/response experiment with Montana soils, we found the lowest dose for a growth reduction of two native Montana grasses (Koeleria macrantha and Festuca idahoensis) by a racemic mixture of (+/-)-catechin that ranged from about 25 to 50 mM, concentrations, orders of magnitude higher than expected in nature. Autoclaving the soil before adding the catechin did not affect the activity of catechin. We found (-)-catechin to be a potent antioxidant, in contrast to a previous claim that it acts as an allelochemical by causing oxidative stress. Our findings suggest that catechin is not a novel weapon of spotted knapweed and that other allelochemical(s) or alternative mechanisms must be found to explain the success of this species as an invader in North America.

No abstract

Cantharidin is a natural compound isolated from the blister beetle (Epicauta spp.). It is a potent inhibitor of protein serine/threonine phosphatases (PPPs), especially PP2A and PP4. Protein phosphatases and kinases maintain a sensitive balance between dephosphorylated and phosphorylated forms of appropriate proteins, thereby playing important roles in signal transduction pathways and regulation of gene expression, cellular proliferation, cell differentiation, apoptosis and other processes. The foliage of 12-day-old Arabidopsis thaliana seedlings was treated with 200 µM (IC(30) ) of the PPP inhibitor cantharidin, and the entire transcriptome profile was determined by microarray analysis at 2, 10 and 24 h after treatment. The transcription of approximately 10% (2577) of the 24 000 genes of Arabidopsis changed significantly (P≤ 0.05 and signal log ratios: ≥1 or ≤-1) after treatment. Inhibition of PPPs significantly reduced transcription of genes associated with auxin and light signaling and induced expression of genes involved in the hypersensitive response and in flagellin and abscisic acid signaling. The great variety of up- and downregulated genes in this microarray experiment implied that cantharidin interfered with the activities of PPPs that interact directly or indirectly with receptors or are located near the beginning of signal transduction pathways. In many cases, PPPs interact with protein complexes of various receptors such as ethylene or light sensors localized in different cell compartments. They function as negative regulators modifying receptor functions, thus altering signaling that influences transcriptional responses.

For a little over a decade, omics methods (transcriptomics, proteomics, metabolomics, and physionomics) have been used to discover and probe the mode of action of both synthetic and natural phytotoxins. For mode of action discovery, the strategy for each of these approaches is to generate an omics profile for phytotoxins with known molecular targets and to compare this library of responses to the responses of compounds with unknown modes of action. Using more than one omics approach enhances the probability of success. Generally, compounds with the same mode of action generate similar responses with a particular omics method. Stress and detoxification responses to phytotoxins can be much clearer than effects directly related to the target site. Clues to new modes of action must be validated with in vitro enzyme effects or genetic approaches. Thus far, the only new phytotoxin target site discovered with omics approaches (metabolomics and physionomics) is that of cinmethylin and structurally related 5-benzyloxymethyl-1,2-isoxazolines. These omics approaches pointed to tyrosine amino-transferase as the target, which was verified by enzyme assays and genetic methods. In addition to being a useful tool of mode of action discovery, omics methods provide detailed information on genetic and biochemical impacts of phytotoxins. Such information can be useful in understanding the full impact of natural phytotoxins in both agricultural and natural ecosystems.

The apicomplexan parasites pathogens such as Plasmodium spp. possess an apicoplast, a plastid organelle similar to those of plants. The apicoplast has some essential plant-like metabolic pathways and processes, making these parasites susceptible to inhibitors of these functions. The main objective of this paper is to determine if phytotoxins with plastid target sites are more likely to be good antiplasmodial compounds than are those with other modes of action. The antiplasmodial activities of some compounds with established phytotoxic action were determined in vitro on a chloroquine (CQ) sensitive (D6, Sierra Leone) strain of Plasmodium falciparum. In this study, we provide in vitro activities of almost 50 such compounds, as well as a few phytoalexins against P. falciparum. Endothall, anisomycin, and cerulenin had sufficient antiplasmodial action to be considered as new lead antimalarial structures. Some derivatives of fusicoccin possessed markedly improved antiplasmodial action than the parent compound. Our results suggest that phytotoxins with plastid targets may not necessarily be better antiplasmodials than those that act at other molecular sites. The herbicides, phytotoxins and the phytoalexins reported here with significant antiplasmodial activity may be useful probes for identification of new antimalarial drug targets and may also be used as new lead structures for new antiplasmodial drug discovery.