Abstract
Arabidopsis FAD7 encodes a plastidial ω-3 desaturase, which catalyzes the production of trienoic fatty acids, the precursors of jasmonic acid (JA). In coordination with other JA-biosynthetic genes, FAD7 is strongly induced by wounding. This constitutes a feedforward mechanism allowing rapid and sustainable JA accumulation. To identify molecular components involved in this mechanism, transgenic Arabidopsis carrying FAD7 promoter fused to firefly luciferase gene (pFAD7-LUC) was constructed. Reciprocal crossing experiments revealed that the FAD7 induction depends on JA biosynthesis and SCFCOI1-mediated signaling, while JA alone is insufficient for maximal induction. It required synergism between JA-dependent and -independent signaling mechanisms. Genetic screen for aberrant pFAD7-LUC expression yielded a recessive wound-hyperresponsive mutant. The mutation was associated with cpl1 locus encoding a C-terminal domain phosphatase of RNA polymerase II, and capable of conferring wound hyperresponsiveness on promoters of several JA-biosynthetic genes. Potential roles of CPL proteins in the attenuation of wound-activated JA biosynthesis are discussed.
