Abstract

The dlm (disease lesion mimic) mutant of soybean (Glycine max L. Merr) shows the similar lesion of a soybean disease caused by a fungus, Corynespora cassilcola. The lesion was examined at cellular and molecular level. Trypan blue staining result indicated that cell death was detectable in the entire region of leaves excluding veins when the lesions had already been developed. We found that the mesophyll cells of palisade layer in the dim mutant appeared to be wider apart from each other. The chloroplasts of the dim mutant cells contained bigger starch granules than those in normal plants. We also found that the lesion development of dlm plant was light-dependent and the starch degradation during the dark period of diurnal cycle was impaired in the mutant. Three soybean pathogenesis-related genes, PR-1a, PR-4, and PR-10, were examined for their expression patterns during the development of disease lesion mimic. The expression of all three genes was up-regulated to some extent upon the appearance of the disease lesion mimic. Although the exact function of DLM protein remains elusive, our data would provide some insight into mechanism underling the cell death associated with the dim mutation.

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