1Faculty of Life and Environmental Science, Shimane University, Matsue 690-8504, Japan; 2National Agricultural Research Center, Tsukuba 305-0035, Japan; 3Faculty of Agriculture, Kobe University, Kobe 657-0013, Japan

Background and objectives
The rice blast fungus Magnaporthe grisea (Hebert) Barr causes the most serious disease of rice. Genetic studies have demonstrated that blast resistance is controlled by several major gene pairs, and resistance against the rice blast fungus differs among cultivars. Resistance or susceptibility of rice plants to M. grisea is determined by race-cultivar combinations. The fungus can also infect other Gramineae such as barley, Italian ryegrass and corn. Thus the rice blast fungus offers an excellent system for studying molecular determinants of host species specificity and cultivar specificity. Host-specific toxins or suppressors are well known as pathogenicity factors of fungal pathogens. In the M. grisea-plant system, however, the pathogenicity factors involved in host susceptibility have not been demonstrated. In earlier work, we reported that M. grisea produces a host-selective toxin during spore germination [1]. In this paper, we report that mitochondrial modifications are the primary effects of the toxin from M. grisea on the ultrastructure of host-plant leaf cells.

Results and conclusions
The toxin of M. grisea was detected in spore germination fluid. When spores of Alternaria alternata, which is not a pathogen of rice, were inoculated in the presence of the toxin, abundant necrotic lesions were formed on rice leaves. The toxin induced susceptibility of rice plants to A. alternata regardless of the compatibility between the races of the blast fungus used to obtain the toxin or the rice cultivars tested. Thus the race-cultivar specificity cannot be explained by the susceptibility-inducing activity of M. grisea toxin. On the other hand, M. grisea also infects some other plants besides rice. The induction of susceptibility by the toxin was also observed on other host plants (e.g. barley, Italian ryegrass, perennial ryegrass and wheat), but not on non-host plants (e.g. corn, crabgrass and finger millet). These results suggest that the toxin is not playing an important role in specificity at the race-cultivar level, but in establishment of basic compatibility at the species level between fungus and plant. The effects of the toxin on the host (rice and barley) and non-host (finger millet) plants were examined by ultrastructural observation and morphometric measurement. The first toxin-induced changes in rice and barley plants were the loss of the mitochondrial matrix and the disruption of mitochondrial cristae. These modifications in mitochondria were observed 1 h after toxin exposure, and the frequency of modified mitochondria did not increase with time after toxin treatment. Morphological and ultrastructural changes were not observed in other organelles. Toxin effects were observed in epidermal, mesophyll and phloem cells of barley and rice but not in leaves of the non-host plant, finger millet. Furthermore, mitochondrial modifications were observed in epidermal cells of rice plants 12 h after inoculation of M. grisea spores. These results indicated that mitochondrial modification induced by the toxin was a host-specific phenomenon and possibly an essential event for M. grisea to establish basic compatibility with host plants at the species level.

1. Arase S, Uehara T, Honda Y et al., 1997. In Kohmoto K, Yoder OC, eds, Molecular Genetics of Host-Specific Toxins in Plant Disease. Kluwer, Dordrecht, in press.