Open AccessNitric Oxide and Reactive Oxygen Species Do Not Elicit Hypersensitive Cell Death but Induce Apoptosis in the Adjacent Cells During the Defense Response of Oat
Author(s) -
Yutaka Tada,
Tomoyo Mori,
Takeshi Shinogi,
Nan Yao,
Satsuki Takahashi,
Shigeyuki Betsuyaku,
Masaru Sakamoto,
Pyoyun Park,
Hitoshi Nakayashiki,
Yukio Tosa,
Shigeyuki Mayama
Publication year - 2004
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi.2004.17.3.245
Subject(s) - dna laddering , hypersensitive response , reactive oxygen species , programmed cell death , apoptosis , nitric oxide , biology , microbiology and biotechnology , superoxide dismutase , superoxide , dna damage , biochemistry , chemistry , oxidative stress , dna fragmentation , dna , enzyme , endocrinology
Nitric oxide (NO) acts as a signaling molecule in many cellular responses in plants and animals. Oat plants (Avena sativa L.) evoke the hypersensitive response (HR), which shares morphological and biochemical features with mammalian apoptosis, such as DNA laddering and heterochromatin condensation, in response to the avirulent crown rust fungus (Puccinia coronata f. sp. avenae). We examined the role of NO and reactive oxygen species (ROS) in the initiation of hypersensitive cell death, which is induced by direct contact with the pathogen, and apoptotic cell death in the adjacent cells. Cytofluorimetric analysis using the fluorescent NO probe DAF and the H 2 O 2 probe DCF demonstrated that NO and H 2 O 2 were generated simultaneously in primary leaves at an early stage of the defense response. The NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) markedly enhanced H 2 O 2 accumulation detected by 3,3-diaminobenzidine staining and DCF, whereas treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) strongly suppressed it. Superoxide dismutase (SOD) increased NO accumulation, suggesting that endogenous NO may modulate the level of H 2 O 2 by interacting with O 2 - in the HR lesion. Cytological observation showed that administration of cPTIO, SNAP, or SOD had no effect on elicitation of hypersensitive cell death, but clearly reduced heterochromatin condensation in the nearby cells and DNA laddering. These findings indicate that NO and ROS are not essential mediators for the initiation of hypersensitive cell death. However, NO and O 2 - but not H 2 O 2 are required for the onset of apoptotic cell death in the adjacent cells, where excess NO may exert its anti-apoptotic function by regulating cellular redox state.