Role of β-oxidation in jasmonate biosynthesis and systemic wound signaling in tomato

被引:244
作者
Li, CY
Schilmiller, AL
Liu, GH
Lee, GI
Jayanty, S
Sageman, C
Vrebalov, J
Giovannoni, JJ
Yagi, K
Kobayashi, Y
Howe, GA [1 ]
机构
[1] Michigan State Univ, Dept Energy, Plant Res Lab, E Lansing, MI 48824 USA
[2] Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA
[3] Cornell Univ, Boyce Thompson Inst Plant Res, Ithaca, NY 14853 USA
[4] Cornell Univ, USDA ARS, US Plant Soil & Nutr Lab, Ithaca, NY 14853 USA
[5] Tokyo Inst Technol, Dept Biol Engn, Midori Ku, Yokohama, Kanagawa 2268501, Japan
关键词
D O I
10.1105/tpc.104.029108
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Jasmonic acid (JA) is a lipid-derived signal that regulates plant defense responses to biotic stress. Here, we report the characterization of a JA-deficient mutant of tomato (Lycopersicon esculentum) that lacks local and systemic expression of defensive proteinase inhibitors (Pis) in response to wounding. Map-based cloning studies demonstrated that this phenotype results from loss of function of an acyl-CoA oxidase (ACX1A) that catalyzes the first step in the peroxisomal beta-oxidation stage of JA biosynthesis. Recombinant ACX1A exhibited a preference for C12 and C14 straight-chain acyl-CoAs and also was active in the metabolism of C18 cyclopentanoid-CoA precursors of JA. The overall growth, development, and reproduction of acx1 plants were similar to wild-type plants. However, the mutant was compromised in its defense against tobacco hornworm (Manduca sexta) attack. Grafting experiments showed that loss of ACX1A function disrupts the production of the transmissible signal for wound-induced PI expression but does not affect the recognition of this signal in undamaged responding leaves. We conclude that ACX1A is essential for the beta-oxidation stage of JA biosynthesis and that JA or its derivatives is required both for antiherbivore resistance and the production of the systemic wound signal. These findings support a role for peroxisomes in the production of lipid-based signaling molecules that promote systemic defense responses.
引用
收藏
页码:971 / 986
页数:16
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