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.
Considerable progress has been made in identifying the targets of plant microRNAs, many of which regulate the stability or translation of mRNAs that encode transcription factors involved in development. In most cases, it is unknown, however, which immediate transcriptional targets mediate downstream effects of the microRNA-regulated transcription factors. We identified a new process controlled by the miR319-regulated clade of TCP (TEOSINTE BRANCHED/CYCLOIDEA/PCF) transcription factor genes. In contrast to other miRNA targets, several of which modulate hormone responses, TCPs control biosynthesis of the hormone jasmonic acid. Furthermore, we demonstrate a previously unrecognized effect of TCPs on leaf senescence, a process in which jasmonic acid has been proposed to be a critical regulator. We propose that miR319-controlled TCP transcription factors coordinate two sequential processes in leaf development: leaf growth, which they negatively regulate, and leaf senescence, which they positively regulate.
Unlike plants, animals rely on rapid nervous systems to escape predation. A stationary fly that perceives danger takes less than 300 ms to take off, and this process requires complex whole- to ion fluxes in cell populations in wounded Arabidopsis plants. As summarised in Supplementary Fig. 1, we show that electrical signalling activates jasmonate biosynthesis in leaves distal to wounds and we identify genes involved in electrical signal propagation. Wound-induced surface potential changesTo investigate patterns of electrical activity and gene expression in 5 week-old rosettes, individual leaves were numbered from oldest to youngest. Electrodes placed on leaf 8 at the midrib/petiole junction (e2 electrode position) and on the petiole (position e3) did not detect changes in electrical activity and such changes were not elicited by walking S. littoralis larvae (Fig. 1b). When recordings were extended, they often showed periodicity ( Supplementary Fig. 3). We used three parameters to characterise these signals: latency (time from wounding to arrival at the amplitude midpoint), amplitude and duration (Fig. 1b). To gain more information on the spread of WASPs within a wounded leaf, four electrodes were placed on the leaf surface (Fig. 1a). After damage, WASPs were detected first at e1, then several seconds later at e2, and finally at e3. An electrode on the lamina also detected damage-elicited electrical activity and, in each case (Fig. 1c), the changes in amplitude were typically close to -70 mV (SupplementaryTable 1). The signals we measured had the same polarity as those produced after a chilling treatment known to cause plasma membrane depolarisation 24,25 . Therefore WASPs in leaf 8 were due to plasma membrane depolarisation ( Supplementary Fig. 4). The WASPs detected on WT plants were indistinguishable to those on wounded plants that lacked the ability to synthesize jasmonates ( Supplementary Fig. 5).This suggests that the mechanism that produces WASPs is upstream or independent of jasmonate synthesis. WASP territories and speedsSignals generated by wounding leaf tips first move towards the centre of the rosette and then disperse away from the apex into a restricted number of distal leaves to initiate distal JA accumulation and signalling 11 . In order to map the spatial distribution of WASPs in the rosette after wounding leaf 8 we placed electrodes in the e3 position of leaves 5 through 18. Leaves 5, 11, 13 and 16 showed responses similar to those in the wounded leaf (Fig. 1d, Supplementary Table 2). For example, after wounding leaf 8, a WASP with a duration of 78±20 s and a peak amplitude of -51 ± 9 mV was reached in leaf 13 after a latency of 66 ± 13 s (n=61 plants). Other leaves (7, 9, 10, 12, 14, 15,17 and 18) showed small positive surface potential changes. For example, leaf 9 showed a 20±5 mV change in surface potential with a latency of 54±12 s (n=46 plants). Most of these observations fit a developmental pattern: In adult-phase Arabidopsis rosettes, leaf 'n' shares direct vascular connections to leave...
Inducible defensive responses in plants are known to be activated locally and systemically by signaling molecules that are produced at sites of pathogen or insect attacks, but only one chemical signal, ethylene, is known to travel through the atmosphere to activate plant defensive genes. Methyl jasmonate, a common plant secondary compound, when applied to surfaces of tomato plants, induces the synthesis of defensive proteinase inhibitor proteins in the treated plants and in nearby plants as well. The presence of methyl jasmonate in the atmosphere of chambers containing plants from three species of two families, Solanaceae and Fabaceae, results in the accumulation of proteinase inhibitors in leaves of all three species. When sagebrush, Artemisia tridentata, a plant shown to possess methyl jasmonate in leaf surface structures, is incubated in chambers with tomato plants, proteinase inhibitor accumulation is induced in the tomato leaves, demonstrating that interplant communication can occur from leaves ofone species of plant to leaves of another species to activate the expression of defensive genes.
Pollination in flowering plants requires that anthers release pollen when the gynoecium is competent to support fertilization. We show that in Arabidopsis thaliana, two paralogous auxin response transcription factors, ARF6 and ARF8, regulate both stamen and gynoecium maturation. arf6 arf8 double-null mutant flowers arrested as infertile closed buds with short petals, short stamen filaments, undehisced anthers that did not release pollen and immature gynoecia. Numerous developmentally regulated genes failed to be induced. ARF6 and ARF8 thus coordinate the transition from immature to mature fertile flowers. Jasmonic acid (JA) measurements and JA feeding experiments showed that decreased jasmonate production caused the block in pollen release, but not the gynoecium arrest. The double mutant had altered auxin responsive gene expression. However, whole flower auxin levels did not change during flower maturation, suggesting that auxin might regulate flower maturation only under specific environmental conditions, or in localized organs or tissues of flowers. arf6 and arf8 single mutants and sesquimutants (homozygous for one mutation and heterozygous for the other) had delayed stamen development and decreased fecundity, indicating that ARF6 and ARF8 gene dosage affects timing of flower maturation quantitatively.
Wounding in multicellular eukaryotes results in marked changes in gene expression that contribute to tissue defense and repair. Using a cDNA microarray technique, we analyzed the timing, dynamics, and regulation of the expression of 150 genes in mechanically wounded leaves of Arabidopsis. Temporal accumulation of a group of transcripts was correlated with the appearance of oxylipin signals of the jasmonate family. Analysis of the coronatine-insensitive coi1-1 Arabidopsis mutant that is also insensitive to jasmonate allowed us to identify a large number of COI1-dependent and COI1-independent wound-inducible genes. Water stress was found to contribute to the regulation of an unexpectedly large fraction of these genes. Comparing the results of mechanical wounding with damage by feeding larvae of the cabbage butterfly (Pieris rapae) resulted in very different transcript profiles. One gene was specifically induced by insect feeding but not by wounding; moreover, there was a relative lack of water stress-induced gene expression during insect feeding. These results help reveal a feeding strategy of P. rapae that may minimize the activation of a subset of water stress-inducible, defense-related genes.
The Arabidopsis opr3 mutant is defective in the isoform of 12-oxophytodienoate (OPDA) reductase required for jasmonic acid (JA) biosynthesis. Oxylipin signatures of wounded opr3 leaves revealed the absence of detectable 3R,7S-JA as well as altered levels of its cyclopentenone precursors OPDA and dinor OPDA. In contrast to JA-insensitive coi1 plants and to the fad3 fad7 fad8 mutant lacking the fatty acid precursors of JA synthesis, opr3 plants exhibited strong resistance to the dipteran Bradysia impatiens and the fungus Alternaria brassicicola. Analysis of transcript profiles in opr3 showed the wound induction of genes previously known to be JA-dependent, suggesting that cyclopentenones could fulfill some JA roles in vivo. Treating opr3 plants with exogenous OPDA powerfully up-regulated several genes and disclosed two distinct downstream signal pathways, one through COI1, the other via an electrophile effect of the cyclopentenones. We conclude that the jasmonate family cyclopentenone OPDA (most likely together with dinor OPDA) regulates gene expression in concert with JA to fine-tune the expression of defense genes. More generally, resistance to insect and fungal attack can be observed in the absence of JA.OPDA reductase ͉ opr3 ͉ Arabidopsis ͉ insect A major objective in plant biology is to develop an integrated understanding of how plants survive in their environment and reproduce. Although it has become clear in the last decade that jasmonic acid (JA) is a key regulator in the development, physiology, and defense of plants, the complexity of the signaling network in which JA evolves is just emerging (1). JA is involved in carbon partitioning (2), in mechanotransduction (3), and the ability of plants to synthesize and perceive JA is absolutely essential for the correct development and release of pollen in Arabidopsis (4-7). Highlighting the regulatory importance of JA, a JA-responsive transcription factor, ORCA3, first found in Catharanthus, provides an important link between primary and secondary metabolism (8). There is also strong evidence supporting a central role of JA in plant defense. Exogenous JA powerfully regulates the expression of many defense genes in plants, and its in vivo production and perception seem to be of vital importance in mounting successful defense against insect attackers (9-11). Together with ethylene, JA also plays a crucial role in defense against necrotrophic fungi (12-14) and in induced systemic resistance in response to nonpathogenic rhizobacteria (15). Broader roles of JA in plant stress responses are likely; it is known that the JA biosynthesis pathway is important in gene activation subsequent to UV damage in plants (16), and JA has been implicated in some responses to water stress (17).The biosynthesis of JA occurs through the octadecanoid pathway (18,19) and is initiated by the addition of molecular oxygen to linolenic acid (18:3) to form 13-hydroperoxylinolenic acid (13-HPOTrE). This fatty acid hydroperoxide is then dehydrated by allene oxide synthase (AOS) and cyclized by ...
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