Cooperation and Functional Diversification of Two Closely Related Galactolipase Genes for Jasmonate Biosynthesis
Youbong Hyun, 1 Sungwook Choi, 1 Hyun-Ju Hwang, 1 Jihyeon Yu, 1 Sang-Jip Nam, 2 Jaeyoung Ko, 2 Ju-Young Park, 3 Young Sam Seo, 4 Eun Yu Kim, 4 Stephen Beungtae Ryu, 5 Woo Taek Kim, 4 Yong-Hwan Lee, 3 Heonjoong Kang, 2 and Ilha Lee 1,6,*
1 National Research Laboratory of Plant Developmental Genetics, Department of Biological Sciences, Seoul National University, Seoul 151-742, Korea 2 School of Earth and Environmental Sciences, Seoul National University, Seoul 151-747, Korea 3 Department of Agricultural Biotechnology, Seoul National University, Seoul 151-921, Korea 4 Department of Biology, College of Science, Yonsei University, Seoul 120-749, Korea 5 Bio-Evaluation Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Chungbuk 363-883, Korea 6 Global Research Laboratory for Flowering at SNU and UW, Seoul 151-742, Korea
*Corresponding author Ilha Lee
Summary
Jasmonic acid (JA) plays pivotal roles in diverse plant biological processes, including wound response. Chloroplast lipid hydrolysis is a critical step for JA biosynthesis, but the mechanism of this process remains elusive. We report here that DONGLE (DGL), a homolog of DEFECTIVE IN ANTHER DEHISCENCE1 (DAD1), encodes a chloroplast-targeted lipase with strong galactolipase and weak phospholipase A1 activity. DGL is expressed in the leaves and has a specific role in maintaining basal JA content under normal conditions, and this expression regulates vegetative growth and is required for a rapid JA burst after wounding. During wounding, DGL and DAD1 have partially redundant functions for JA production, but they show different induction kinetics, indicating temporally separated roles: DGL plays a role in the early phase of JA production, and DAD1 plays a role in the late phase of JA production. Whereas DGL and DAD1 are necessary and sufficient for JA production, phospholipase D appears to modulate wound response by stimulating DGL and DAD1 expression.
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