Tomato susceptibility to Alternaria stem canker:Parameters involved in host-specific toxin-induced leaf necrosis

AAL-toxin causes severe necrosis in leaves of susceptible tomato cultivars at nanomolar concentrations. In resistant tomato cultivars harbouring the semi-dominant Alternaria stem canker resistance locus necrosis is also observed, however at much higher toxin concentrations, in both lines the percentage of the leaf area exhibiting necrosis is dependent on toxin concentration and on length of toxin exposure. However, at the same toxin concentration, periods of toxin exposure resulting in similar necrosis are much longer for the resistant than for the susceptible tomato. It was demonstrated that toxin uptake in the leaves does not imply toxin uptake in the cells since a discrepancy was observed between death of protoplasts, isolated from leaves cut for protoplast isolation immediately after incubation on AAL-toxin and necrosis in leaves when further incubated on water. However, when after exposure to AAL-toxin leaves were further incubated on water for 24 h before they were cut for protoplast isolation, a correlation was found between leaf necrosis and death of protoplasts. This suggests that further transport is needed in leaves after toxin uptake, bringing toxin to all the cells, that cannot occur in leaves cut for protoplast isolation. Light plays an important role in AAL-toxin induced necrosis and it was shown that length of light exposure controls necrosis development like toxin concentration and length of toxin exposure. The product of these 3 parameters can provide a good hint to predict the extent of leaf necrosis. The effect of light might be restricted to differentiated leaf tissue, since it was not observed in callus tissue

Tomato susceptibility to Alternaria stem canker: Parameters involved in host-specific toxin-induced leaf necrosis

AAL-toxin causes severe necrosis in leaves of susceptible tomato cultivars at nanomolar concentrations. In resistant tomato cultivars harbouring the semi-dominant Alternaria stem canker resistance locus necrosis is also observed, however at much higher toxin concentrations, in both lines the percentage of the leaf area exhibiting necrosis is dependent on toxin concentration and on length of toxin exposure. However, at the same toxin concentration, periods of toxin exposure resulting in similar necrosis are much longer for the resistant than for the susceptible tomato. It was demonstrated that toxin uptake in the leaves does not imply toxin uptake in the cells since a discrepancy was observed between death of protoplasts, isolated from leaves cut for protoplast isolation immediately after incubation on AAL-toxin and necrosis in leaves when further incubated on water. However, when after exposure to AAL-toxin leaves were further incubated on water for 24 h before they were cut for protoplast isolation, a correlation was found between leaf necrosis and death of protoplasts. This suggests that further transport is needed in leaves after toxin uptake, bringing toxin to all the cells, that cannot occur in leaves cut for protoplast isolation. Light plays an important role in AAL-toxin induced necrosis and it was shown that length of light exposure controls necrosis development like toxin concentration and length of toxin exposure. The product of these 3 parameters can provide a good hint to predict the extent of leaf necrosis. The effect of light might be restricted to differentiated leaf tissue, since it was not observed in callus tissue.

Effects of Alternaria alternata f.sp. lycopersici Toxins at Different Levels of Tomato Plant Cell Development

Since the host-specific toxins of Alternaria alternata f. sp. lycopersici play an important role in pathogenesis, they potentially could be applied as selective agents in in vitro selection at the cellular level for disease resistance. Prerequisite for this is that sensitivity to the Alternaria alternata f.sp. lycopersici pathotoxins is manifest at the cellular level. To gain insight into cellular effects of AAL-toxins and into the mechanisms of plant insensitivity to AAL-toxins, effects of AAL-toxins on leaves, leaf discs, roots, calli, suspension cells, minicalli and protoplasts of susceptible and resistant tomato genotypes were studied. In leaves of susceptible genotypes, toxins cause severe necrosis, while in leaves of resistant genotypes necrosis was never observed. Inhibition effects of toxins were observed at all other levels in susceptible and resistant genotypes: toxins inhibited shoot induction on leaf discs, root growth and growth of calli, suspension cells and protoplasts. This indicates a cellular site for AAL-toxins. Differences in sensitivity to AAL-toxins between susceptible and resistant genotypes were observed in leaves and roots, but were not observed during shoot induction on leaf discs, in calli, suspension cells and protoplasts. However, differences in sensitivity to AAL-toxins in roots were at least 20 times less than in leaves. Therefore insensitivity seems related to a higher level of tomato plant differentiation and is most pronounced in leaves.