The Arabidopsis gene CAD1 controls programmed cell death in the plant immune system and encodes a protein containing a MACPF domain

To clarify the processes involved in plant immunity, we have isolated and characterized a single recessive Arabidopsis mutant, cad1 (constitutively activated cell death 1), which shows a phenotype that mimics the lesions seen in the hypersensitive response (HR). This mutant shows spontaneously activ...

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Published in:Plant and cell physiology Vol. 46; no. 6; pp. 902 - 912
Main Authors: Morita Yamamuro, C.(Hokkaido Univ., Sapporo (Japan)), Tsutsui, T, Sato, M, Yoshioka, H, Tamaoki, M, Ogawa, D, Matsuura, H, Yoshihara, T, Ikeda, A, Uyeda, I, Yamaguchi, J
Format: Journal Article
Language:English
Published: Japan Oxford University Press 01-06-2005
Oxford Publishing Limited (England)
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Summary:To clarify the processes involved in plant immunity, we have isolated and characterized a single recessive Arabidopsis mutant, cad1 (constitutively activated cell death 1), which shows a phenotype that mimics the lesions seen in the hypersensitive response (HR). This mutant shows spontaneously activated expression of pathogenesis-related (PR) genes, and leading to a 32-fold increase in salicylic acid (SA). Inoculation of cad1 mutant plants with Pseudomonas syringae pv tomato DC3000 shows that the cad1 mutation results in the restriction of bacterial growth. Cloning of CADI reveals that this gene encodes a protein containing a domain with significant homology to the MACPF (membrane attack complex and perforin) domain of complement components and perforin proteins that are involved in innate immunity in animals. Furthermore, cell death is suppressed in transgenic cad1 plants expressing nahG, which encodes an SA-degrading enzyme. We therefore conclude that the CAD1 protein negatively controls the SA-mediated pathway of programmed cell death in plant immunity.
Bibliography:F60
2006002959
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istex:268DB62E314262F342621FC69CC14DEAD9B57FF2
6Corresponding author: E-mail, jjyama@sci.hokudai.ac.jp; Fax, +81-11-706-2737.
local:pci095
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ISSN:0032-0781
1471-9053
DOI:10.1093/pcp/pci095