growth), cause necrotic lesions (cell death) or wilting of plants. The toxins are low molecular weight secondary metabolites (e.g., polyketide, cyclic tetrapeptide, sesquiterpene epoxide) that are not essential for normal growth and reproduction of fungi. For its growth the fungus uses the leakage of electrolytes, sugars and amino acids from the killed host cells. A common procedure in work with toxins is to grow the parasite in culture and see if purified extracts from the cultures applied at concentrations that could be reasonably expected in the diseased plant reproduce some of the disease symptoms caused by the parasite.
Victorin is a toxin produced by Cochliobolus heterostrophus (Ascomycotina), the causal agent of Victoria blight of oats active at picomolar concentrations and exhibits the same specificity toward oat genotypes as the fungus (Navarre and Wolpert, 1999). It is therefore a host-selective plant toxin and is a cyclized pentapeptide of 814 Dalton. Leaves treated with victorin exhibit cleavage of a photosynthetic carbon-dioxide fixing enzyme, ribulose-1,5-bisphosphate carboxylase (Rubisco), and loss of chlorophyll. In addition, victorin-treated leaves show DNA laddering — cleavage into discrete sizes—characteristic of apoptosis or programmed cell death, suggesting that victorin causes premature senescence of leaves. Mycosphaerella zeae-maydis (Ascomycotina) produces a family of long-chain (C35 to C41) polyketides, called T-toxin and PM-toxin, respectively. The T-toxin specifically affects mitochondria of cultivar carrying the Texas cytoplasmic gene introduced to simplify the production of hybrid varieties. However, mitochondria of normal maize (corn) are not affected by T-toxin. The binding of the toxin to a mitochondrial membrane protein causes pores to form in mitochondrial membranes, resulting in leakage of respiratory substrates, cessation of ATP production and cell death.
The identification of biosynthetic pathways of toxin production, the isolation of toxin non-producing mutants and the development of DNA-mediated transformation of pathogenic fungal species should provide critical proof for the role of toxins in pathogenesis (Desjardins and Hohn, 1997).
Was this article helpful?