|In Leea, Gyu|
Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/1/2005
Publication Date: 3/15/2005
Citation: Lia, C., Liua, G., Schilmillera, A., In Leea, G., Jayantya, S., Sagemana, C., Vrebalov, J., Giovannoni, J.J., Howe, G. 2005. Role of - oxidation in jasmonate biosynthesis and systemic wound signaling in tomato. The Plant Cell. 17:971-986. Interpretive Summary: Jasmonic acid (JA) and its precursors and derivatives, collectively referred to as jasmonates (JAs), constitute a family of bioactive compounds that regulate plant responses to environmental and developmental cues. JAs are perhaps best known for their role in orchestrating plant defense responses to herbivores and certain microbial pathogens. Here, we describe the characterization of a wound-response mutant of tomato that is deficient in JA biosynthesis. Cloning experiments demonstrated that this defect results from loss of function of a member (ACX1) of the ACX family of enzymes that participate in peroxisomal (-oxidation. Results obtained from characterization of acx1 plants advance our knowledge of jasmonate signaling in several ways. First, we show that (-oxidation is necessary for JA biosynthesis, and that a single form of ACX catalyzes the vast majority of wound-induced JA in tomato leaves. Second, we demonstrate that JA is indeed the physiological signal for induced defense responses to insect attack. Finally, grafting experiments indicate that the peroxisomal (-oxidation stage of JA biosynthesis is required for the production of the transmissible wound signal. These findings support the notion that JA is an essential component of the long-distance signal for induced resistance to herbivores.
Technical Abstract: Jasmonic acid (JA) and its C18 precursor, 12-oxo-phytodienoic acid, are fatty acid-derived signaling compounds that regulate plant responses to biotic stress. Here, we report the characterization of a JA-deficient mutant of tomato that lacks local and systemic expression of defensive proteinase inhibitors (PIs) in response to wounding. Map-based cloning studies demonstrate that this phenotype results from loss of function of an acyl-CoA oxidase (ACX1) that catalyzes the first step in the peroxisomal (-oxidation stage of JA biosynthesis. Although the overall growth, development, and reproduction of acx1 plants were similar to wild-type plants, the mutant was compromised in its defense against tobacco hornworm attack. Grafting experiments demonstrate that loss of ACX1 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 (-oxidation is essential for wound-induced JA biosynthesis, and that JA, rather than its C18 precursors, is required both for anti-herbivore resistance and the production of the systemic wound signal. Our results further suggest that peroxisomes are an important source of signaling molecules that promote systemic defense responses.