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Leucine Aminopeptidase RNAs, Proteins, and Activities Increase in Response to Water Deficit, Salinity, and the Wound Signals Systemin, Methyl Jasmonate, and Abscisic Acid1

Wun S. Chao2, Yong-Qiang Gu3, Véronique Pautot, Elizabeth A. Bray, and Linda L. Walling*

Department of Botany and Plant Sciences and the Interdepartmental Program in Genetics, University of California, Riverside, California 92521-0124 (W.S.C., Y.-Q.G., E.A.B., L.L.W.); and Laboratoire de Biologie Cellulaire, Institut National de la Recherche Agronomique, 78026 Versailles cédex, France (V.P.)

LapA RNAs, proteins, and activities increased in response to systemin, methyl jasmonate, abscisic acid (ABA), ethylene, water deficit, and salinity in tomato (Lycopersicon esculentum). Salicylic acid inhibited wound-induced increases of LapA RNAs. Experiments using the ABA-deficient flacca mutant indicated that ABA was essential for wound and systemin induction of LapA, and ABA and systemin acted synergistically to induce LapA gene expression. In contrast, pin2 (proteinase inhibitor 2) was not dependent on exogenous ABA. Whereas both LapA and le4 (L. esculentum dehydrin) were up-regulated by increases in ABA, salinity, and water deficit, only LapA was regulated by octadecanoid pathway signals. Comparison of LapA expression with that of the PR-1 (pathogenesis-related 1) and GluB (basic beta -1,3-glucanase) genes indicated that these PR protein genes were modulated by a systemin-independent jasmonic acid-signaling pathway. These studies showed that at least four signaling pathways were utilized during tomato wound and defense responses. Analysis of the expression of a LapA1:GUS gene in transgenic plants indicated that the LapA1 promoter was active during floral and fruit development and was used during vegetative growth only in response to wounding, Pseudomonas syringae pv tomato infection, or wound signals. This comprehensive understanding of the regulation of LapA genes indicated that this regulatory program is distinct from the wound-induced pin2, ABA-responsive le4, and PR protein genes.

1   This research was supported by a National Science Foundation grant (no. IBN-9318260) to L.L.W. W.S.C. was partially supported by the National Science Foundation training grant (no. GER-5355042).
2   Present address: Department of Botany, Washington State University, Pullman, WA 99164-4238.
3   Present address: Boyce Thompson Institute, Cornell University, Ithaca, New York 14853-1801.
*   Corresponding author; e-mail lwalling{at}citrus.ucr.edu; fax 909-787-4437.

Plant Physiol. (1999) 120: 979-992
Copyright Clearance Center:   0032-0889/99/120//14
© 1999 American Society of Plant Physiologists




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