Nitric oxide Does Not Trigger Early Programmed Cell Death Events but May Contribute to Cell-to-Cell Signaling Governing Progression of the Arabidopsis Hypersensitive Response

Nitric oxide (NO) has been suggested to play a role in the hypersensitive response (HR). Single- and double-label fluorescence microscopy experiments were conducted using Arabidopsis leaves infected with Pseudomonas syringae pv. tomato DC3000 carrying either avrB or avrRpt2. Kinetics of NO productio...

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Published in:	Molecular plant-microbe interactions Vol. 16; no. 11; pp. 962 - 972
Main Authors:	Zhang, Chu, Cymmek, Kirk J, Shapiro, Allan D
Format:	Journal Article
Language:	English
Published:	St Paul, MN APS Press 01-11-2003 American Phytopathological Society The American Phytopathological Society
Subjects:	apoptosis Apoptosis - drug effects Apoptosis - physiology Arabidopsis Arabidopsis - cytology Arabidopsis - drug effects Arabidopsis - microbiology Arabidopsis - physiology Biological and medical sciences Biological Transport disease resistance fluorescence fluorescence microscopy Fundamental and applied biological sciences. Psychology hypersensitive response leaves mutants nitric oxide Nitric Oxide - metabolism Nitric Oxide - pharmacology nitric oxide synthase Nitric Oxide Synthase - metabolism Phytopathology. Animal pests. Plant and forest protection Plant Diseases - microbiology Plant Leaves - cytology Plant Leaves - drug effects Plant Leaves - physiology propidium Pseudomonas syringae - pathogenicity Pseudomonas syringae pv. tomato signal transduction Signal Transduction - drug effects Signal Transduction - physiology triazoles Microbiology Cruciferae Arabidopsis Cell death Dicotyledones Nitric oxide Angiospermae Spermatophyta
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Summary:	Nitric oxide (NO) has been suggested to play a role in the hypersensitive response (HR). Single- and double-label fluorescence microscopy experiments were conducted using Arabidopsis leaves infected with Pseudomonas syringae pv. tomato DC3000 carrying either avrB or avrRpt2. Kinetics of NO production were followed by measurement of green 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM) triazole fluorescence in leaves coinfiltrated with DAF-FM diacetate. Kinetics of hypersensitive cell death were followed by measurement of cytoplasmic red fluorescence following internalization of coinfiltrated propidium iodide through compromised plasma membranes. Neither NO accumulation nor cell death was seen until approximately 3 h postinoculation of Columbia leaves with DC3000·avrB or approximately 5.5 h post-inoculation with DC3000·avrRpt2. Subsequent NO accumulation kinetics closely paralleled HR progression in both Columbia and ndr1-1 mutant plants. These data established that NO accumulation does not happen sufficiently early for NO to be a signaling component controlling HR triggering. NO accumulation did contribute to the HR, as proven by an approximately 1-h delay in cell death kinetics caused by an NO scavenger or an NO synthase inhibitor. NO was first seen as punctate foci at the cell surface. Subsequent NO accumulation patterns were consistent with NO being an intercellular signal that functions in cell-to-cell spread of the HR.
Bibliography:	http://dx.doi.org/10.1094/MPMI.2003.16.11.962 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0894-0282 1943-7706
DOI:	10.1094/MPMI.2003.16.11.962