Wounding plant tissues initiates large-scale changes in transcription coupled to growth arrest, allowing resource diversion for defense. These processes are mediated in large part by the potent lipid regulator jasmonic acid (JA). Genes selected from a list of wound-inducible transcripts regulated by the jasmonate pathway were overexpressed in Arabidopsis thaliana, and the transgenic plants were then assayed for sensitivity to methyl jasmonate (MeJA). When grown in the presence of MeJA, the roots of plants overexpressing a gene of unknown function were longer than those of wild-type plants. When transcript levels for this gene, which we named JASMONATE-ASSOCIATED1 (JAS1), were reduced by RNA interference, the plants showed increased sensitivity to MeJA and growth was inhibited. These gain-and loss-of-function assays suggest that this gene acts as a repressor of JA-inhibited growth. An alternative transcript from the gene encoding a second protein isoform with a longer C terminus failed to repress jasmonate sensitivity. This identified a conserved C-terminal sequence in JAS1 and related genes, all of which also contain Zim motifs and many of which are jasmonate-regulated. Both forms of JAS1 were found to localize to the nucleus in transient expression assays. Physiological tests of growth responses after wounding were consistent with the fact that JAS1 is a repressor of JA-regulated growth retardation.

A new metabolite profiling approach combined with an ultrarapid sample preparation procedure was used to study the temporal and spatial dynamics of the wound-induced accumulation of jasmonic acid (JA) and its oxygenated derivatives in Arabidopsis thaliana. In addition to well known jasmonates, including hydroxyjasmonates (HOJAs), jasmonoyl-isoleucine (JA-Ile), and its 12-hydroxy derivative (12-HOJA-Ile), a new wound-induced dicarboxyjasmonate, 12-carboxyjasmonoyl-L-isoleucine (12-HOOCJA-Ile) was discovered. HOJAs and 12-HOOCJA-Ile were enriched in the midveins of wounded leaves, strongly differentiating them from the other jasmonate metabolites studied. The polarity of these oxylipins at physiological pH correlated with their appearance in midveins. When the time points of accumulation of different jasmonates were determined, JA levels were found to increase within 2-5 min of wounding. Remarkably, these changes occurred throughout the plant and were not restricted to wounded leaves. The speed of the stimulus leading to JA accumulation in leaves distal to a wound is at least 3 cm/min. The data give new insights into the spatial and temporal accumulation of jasmonates and have implications in the understanding of long-distance wound signaling in plants.

The wound response prohormone jasmonic acid (JA) accumulates rapidly in tissues both proximal and distal to injury sites in plants. Using quantitative liquid chromatography-mass spectrometry after flash freezing of tissues, we found that JA accumulated within 30 s of injury in wounded Arabidopsis leaves (p ‫؍‬ 3.5 e ؊7 ). JA augmentation distal to wounds was strongest in unwounded leaves with direct vascular connections to wounded leaves wherein JA levels increased significantly within 120 s of wounding (p ‫؍‬ 0.00027). This gave conservative and statistically robust temporal boundaries for the average velocity of the long distance signal leading to distal JA accumulation in unwounded leaves of 3.4 -4.5 cm min ؊1 . Like JA, transcripts of the JA synthesis gene LIPOXYGENASE2 (LOX2) and the jasmonate response gene JAZ10.3 also accumulated to higher levels in directly interconnected leaves than in indirectly connected leaves. JA accumulation in a lox2-1 mutant plant was initiated rapidly after wounding then slowed progressively compared with the wild type (WT). Despite this, JAZ10.3 expression in the two genotypes was similar. Free cyclopentenone jasmonate levels were similar in both resting WT and lox2-1. In contrast, bound cyclopentenone jasmonates (arabidopsides) were far lower in lox2-1 than in the WT. The major roles of LOX2 are to generate arabidopsides and the large levels of JA that accumulate proximal to the wound. LOX2 is not essential for some of the most rapid events elicited by wounding.

Plants possess a family of potent fatty acid-derived wound-response and developmental regulators: the jasmonates. These compounds are derived from the tri-unsaturated fatty acids alpha-linolenic acid (18:3) and, in plants such as Arabidopsis thaliana and tomato, 7(Z)-, 10(Z)-, and 13(Z)-hexadecatrienoic acid (16:3). The lipoxygenase-catalyzed addition of molecular oxygen to alpha-linolenic acid initiates jasmonate synthesis by providing a 13-hydroperoxide substrate for formation of an unstable allene oxide by allene oxide synthase (AOS). This allene oxide then undergoes enzyme-guided cyclization to produce 12-oxophytodienoic acid (OPDA). These first steps take place in plastids, but further OPDA metabolism occurs in peroxisomes. OPDA has several fates, including esterification into plastid lipids and transformation into the 12-carbon prohormone jasmonic acid (JA). JA is itself a substrate for further diverse modifications, including the production of jasmonoyl-isoleucine (JA-Ile), which is a major biologically active jasmonate among a growing number of jasmonate derivatives. Each new jasmonate family member that is discovered provides another key to understanding the fine control of gene expression in immune responses; in the initiation and maintenance of long-distance signal transfer in response to wounding; in the regulation of fertility; and in the turnover, inactivation, and sequestration of jasmonates, among other processes.

In higher plants such as Arabidopsis thaliana, omega-3 trienoic fatty acids (TFAs), represented mainly by ␣-linolenic acid, serve as precursors of jasmonic acid (JA), a potent lipid signal molecule essential for defense. The JA-independent roles of TFAs were investigated by comparing the TFA-and JA-deficient fatty acid desaturase triple mutant (fad3-2 fad7-2 fad8 (fad3 fad7 fad8)) with the aos (allene oxide synthase) mutant that contains TFAs but is JA-deficient. When challenged with the fungus Botrytis, resistance of the fad3 fad7 fad8 mutant was reduced when compared with the aos mutant, suggesting that TFAs play a role in cell survival independently of being the precursors of JA. An independent genetic approach using the lesion mimic mutant accelerated cell death2 (acd2-2) confirmed the importance of TFAs in containing lesion spread, which was increased in the lines in which the fad3 fad7 fad8 and acd2-2 mutations were combined when compared with the aos acd2-2 lines. Malondialdehyde, found to result from oxidative TFA fragmentation during lesion formation, was measured by gas chromatography-mass spectrometry. Its levels correlated with the survival of the tissue. Furthermore, plants lacking TFAs overproduced salicylic acid (SA), hydrogen peroxide, and transcripts encoding several SA-regulated and SA biosynthetic proteins. The data suggest a physiological role for TFAs as sinks for reactive oxygen species.

The jasmonate signal pathway is known to control defenses against herbivores, such as leaf eaters (folivores). Does the reach of the pathway extend to defense against other types of animal? Among the arthropods attracted to seed baits placed below flowering Arabidopsis thaliana plants are 2 largely nocturnal isopod crustaceans generally considered as detritivores: Porcellio scaber and Armadillidium vulgare. Parallel laboratory experiments identified the isopods as being capable of predation on intact plants. Isopod feeding was strongly facilitated in jasmonate-deficient Arabidopsis and rice plants. The feeding activity of isopods revealed potentially detritivore-sensitive, jasmonate-protected Achilles' heels in these architecturally different plants (petioles and inflorescence stems in Arabidopsis, and lower stem and mesocotyl in rice). The work addresses the question of what stops 2 detritivores from attacking living plants and provides evidence that it is, in part, the jasmonate signal pathway. Furthermore, senescent leaves from an Arabidopsis jasmonate mutant were consumed more rapidly than senescent wild-type leaves, suggesting that past activity of the jasmonate signal pathway in leaves may slow carbon recycling through detritivory.detritivory ͉ isopods ͉ jasmonic acid ͉ plant defense ͉ senescence H erbivory is one of the most important processes in the biosphere, whereby carbon fixed by plants is transferred to higher trophic levels (1, 2). In many cases the largest category of herbivores on the vegetative tissues of plants tends to be insects (3). Additionally, many organisms are known to prey on seeds or otherwise affect seed fate (4). However, herbivores are not the only organisms associated with plants, and only a proportion of the animals associated with plants eat living plant tissues. Another important category of organisms found associated with plants are the detritivores: feeders on dead and dying material (5). Detritivory of plant material is a second major environmental process releasing carbon from plants to higher trophic levels. Like herbivory, this is one of the truly large-scale processes in nature. Detritivores, generally considered apart from herbivores, may actively survey the plant and its vicinity looking for senescent, decaying, or otherwise compromised plant tissues. Furthermore, there is no clear division in nature between detritivory and herbivory, and many arthropods are omnivores feeding at more than one trophic level (6). It is possible that some detritivores, if given the opportunity, might be facultative herbivores. Indeed, it is conceivable that defense barriers against detritivores would be provided by the jasmonate signal pathway, because this pathway operates on the expression of hundreds of wound-inducible defense and survival genes (7) and underlies a major defense system against many herbivores (8).Through field observations we first identified arthropods potentially capable of devouring Arabidopsis seeds. These were early-stage juveniles of the nocturnal dermapteran (e...