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Tryptamine Pathway‐mediated DNA Fragmentation is Involved in Sekiguchi Lesion Formation for Light‐enhanced Resistance in Lesion Mimic Mutant of Rice to Magnaporthe grisea Infection
Author(s) -
Ueno Makoto,
Imaoka Atsuko,
Kihara Junichi,
Arase Sakae
Publication year - 2008
Publication title -
journal of phytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.53
H-Index - 60
eISSN - 1439-0434
pISSN - 0931-1785
DOI - 10.1111/j.1439-0434.2008.01436.x
Subject(s) - magnaporthe grisea , tryptamine , dna fragmentation , biology , mutant , fragmentation (computing) , dna damage , microbiology and biotechnology , dna , biochemistry , gene , programmed cell death , oryza sativa , apoptosis , ecology
In this study, the correlation between tryptamine pathway‐mediated Sekiguchi lesion formation and DNA fragmentation in the sl mutant infected with Magnaporthe grisea under light was investigated. DNA fragmentation was observed beginning at 12 h after M. grisea inoculation, and then increased with increasing time after inoculation under light, but not in the dark. However, in cycloheximide (CHX)‐ or heat shock (HS)‐pretreated leaves of the sl mutant, Sekiguchi lesion formation and DNA fragmentation were significantly inhibited, but not in chloramphenicol (CP)‐pretreated leaves. Tryptamine accumulation and enzyme activity such as tryptophan decarboxylase (TDC) and monoamine oxidase (MAO) were also inhibited, even under light in the CHX‐ or HS‐pretreated leaves, but not in the CP‐pretreated ones. DNA fragmentation and TDC gene expression were induced in the leaves by the treatment with tryptamine or H 2 O 2 under light, but not in the presence of the MAO inhibitor and H 2 O 2 scavenger. The suppressive and inducible effects of biotic and abiotic agents on the induction of DNA fragmentation in the leaves of the sl mutant agree well with those effects on the activation of the tryptamine pathway involved in Sekiguchi lesion formation. These results suggested that tryptamine pathway‐mediated DNA fragmentation induces Sekiguchi lesion formation, which is responsible for light‐enhanced resistance in the sl mutant infected with M. grisea under light.