Relative contribution of LOX10, green leaf volatiles and JA to wound-induced local and systemic oxylipin and hormone signature in Zea mays (maize)

Green leaf volatiles (GLVs) and jasmonates (JAs) are the best-characterized groups of fatty acid-derived oxylipin signals that regulate wound-associated defenses. Beyond these two major groups of defense signals, plants produce an array of oxylipins in response to wounding, which possess potent signaling and/or insecticidal activities. In this study, we assessed the relative contribution of JAs and GLVs to wound-induced systemic signaling and the associated regulation of oxylipins in local and systemic tissues of maize (Zea mays). For this, we utilized GLV- and JA-deficient mutants, lox10 single and opr7opr8 double mutants, respectively, and profiled oxylipins in untreated leaves and roots, and in locally wounded and systemic leaves. In contrast to the studies in dicots, no systemic induction of JAs was observed in maize. Instead, a JA precursor, 12-OPDA, as well as ketols and C12/13 oxo-acids derived from 13-lipoxygenases (LOXs), were preferentially induced in both locally wounded and systemic unwounded leaves. Several 9-LOX-derived oxylipins (9-oxylipins) including hydroxides and ketones were also significantly induced locally. JA and JA-isoleucine (JA-Ile) were rapidly induced within 0.5 h, and were followed by a second increase in local tissue 4 h after wounding. GLV-deficient lox10 mutants displayed reduced levels of most 13-oxylipins, and elevated levels of several 9-oxylipins and the a-dioxygenase (DOX) product, 2-HOD. lox10 mutants were completely devoid of C6 volatiles and their C12 counterparts, and greatly decreased in C5 volatiles and their C13 oxo-acid counterparts. Thus, in addition to being the sole LOX isoform providing substrate for GLV synthesis, LOX10 is a major 13-LOX that provides substrate to several LOX branches that produce an array of 13-oxylipin products, including C5 volatiles. Interestingly, the rapid JA and JA-Ile increase at 0.5–2 h post-wounding was only moderately affected by the LOX10 mutation, while significantly reduced levels were observed at 4 h post-wounding. Combined with the previous findings that GLVs activate JA biosynthesis, these results suggest that both LOX10-derived substrates and/or GLVs are involved in the large second phase of JA synthesis proximal to the wound. Analyses of opr7opr8 mutants revealed that wound-induced oxylipin responses were positively regulated by JA signaling. The local and systemic accumulation of SA was not altered in the two mutants. Collectively, our results identified a subset of oxy