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First published online February 18, 2005; 10.1105/tpc.104.029108

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The Plant Cell 17:971-986 (2005)
© 2005 American Society of Plant Biologists

Role of ß-Oxidation in Jasmonate Biosynthesis and Systemic Wound Signaling in Tomato{boxw}

Chuanyou Lia,1,2, Anthony L. Schilmillera,b,1, Guanghui Liua, Gyu In Leea,3, Sastry Jayantya, Carolyn Sagemana, Julia Vrebalovc, James J. Giovannonic,d, Kaori Yagie, Yuichi Kobayashie and Gregg A. Howea,b,4

a Department of Energy–Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
b Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824
c Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, New York 14853
d U.S. Department of Agriculture–Agricultural Research Service, Plant, Soil, and Nutrition Lab, Cornell University, Ithaca, New York 14853
e Department of Biological Engineering, Tokyo Institute of Technology, 4259-B52 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan 4259

4 To whom correspondence should be addressed. E-mail howeg{at}msu.edu; fax 517-353-9168.

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 ß-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 ß-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.




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