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First published online April 23, 2008; 10.1104/pp.108.119321 Plant Physiology 147:696-706 (2008) © 2008 American Society of Plant Biologists
Induction of the Arabidopsis PHO1;H10 Gene by 12-Oxo-Phytodienoic Acid But Not Jasmonic Acid via a CORONATINE INSENSITIVE1-Dependent Pathway1Département de Biologie Moléculaire Végétale, Biophore, Université de Lausanne, CH–1015 Lausanne, Switzerland
Expression of AtPHO1;H10, a member of the Arabidopsis (Arabidopsis thaliana) PHO1 gene family, is strongly induced following numerous abiotic and biotic stresses, including wounding, dehydration, cold, salt, and pathogen attack. AtPHO1;H10 expression by wounding was localized to the cells in the close vicinity of the wound site. AtPHO1;H10 expression was increased by application of the jasmonic acid (JA) precursor 12-oxo-phytodienoic acid (OPDA), but not by JA or coronatine. Surprisingly, induction of AtPHO1;H10 by OPDA was dependent on the presence of CORONATINE INSENSITIVE1 (COI1). The induction of AtPHO1;H10 expression by wounding and dehydration was dependent on COI1 and was comparable in both the wild type and the OPDA reductase 3-deficient (opr3) mutant. In contrast, induction of AtPHO1;H10 expression by exogenous abscisic acid (ABA) was independent of the presence of either OPDA or COI1, but was strongly decreased in the ABA-insensitive mutant abi1-1. The involvement of the ABA pathway in regulating AtPHO1;H10 was distinct between wounding and dehydration, with induction of AtPHO1;H10 by wounding being comparable to wild type in the ABA-deficient mutant aba1-3 and abi1-1, whereas a strong reduction in AtPHO1;H10 expression occurred in aba1-3 and abi1-1 following dehydration. Together, these results reveal that OPDA can modulate gene expression via COI1 in a manner distinct from JA, and independently from ABA. Furthermore, the implication of the ABA pathway in coregulating AtPHO1;H10 expression is dependent on the abiotic stress applied, being weak under wounding but strong upon dehydration.
Jasmonates, which include jasmonic acid (JA) and its methyl ester (MeJA), act as plant growth regulators and signal molecules involved in numerous development processes and responses to the environment (Farmer et al., 2003  ; Devoto and Turner, 2005; Schilmiller and Howe, 2005; Wasternack, 2007; Browse and Howe, 2008). A prominent role of jasmonates has been described in the response of plants to wounding, pathogen attack as well as water stress and UV damage. JA is also essential in anther development (Feys et al., 1994; Stinzi and Browse, 2000; He et al., 2002).
JA biosynthesis occurs through the octadecanoic acid pathway and is initiated by the oxidation of
Several components of the JA-mediated signal transduction cascade have been characterized. One key component is CORONATINE INSENSITIVE1 (COI1). COI1 contains an F-box domain and associates with Skp-like proteins, cullin, and AtRbx1, a RING-box 1 protein to form an active SCFCOI1 complex that is thought to function as an E3-type ubiquitin ligase (Xu et al., 2001
Apart from being a precursor to JA, OPDA has been found to be an active signal molecule. Transient increase of both OPDA and JA has been described in response to wounding and osmotic stress (Kramell et al., 2000
Numerous responses of plants that are mediated by jasmonates, such as wounding or defense against pathogens, are also influenced by other hormones that may interact in an antagonistic or synergistic fashion depending on the stress or developmental process (Lorenzo and Solano, 2005
This study describes the response of one member of the PHO1 gene family in Arabidopsis to biotic and abiotic stresses. PHO1 is involved in the transfer of phosphate to the xylem in the root, and the Arabidopsis genome contains 10 additional genes showing homology to PHO1 (named AtPHO1;H1 to AtPHO;H10; Poirier et al., 1991
AtPHO1;H10 Is Regulated by Numerous Biotic and Abiotic Stresses Analysis by RNA gel-blot analysis of the expression of the AtPHO1;H10 gene in soil-grown plants revealed that the gene was well expressed in roots and flowers but weakly in leaves and the inflorescence stems (Fig. 1A ). A similar stronger expression in roots compared to leaves was observed for plants grown in agar-solidified medium (Fig. 1A). In transgenic plants expressing the GUS reporter gene under the control of 1.0 kb of the AtPHO1;H10 promoter sequence (pH10::GUS line), strong GUS expression was evident in the epidermal and cortical cells of the roots, particularly in the primary roots and more weakly in the emerging secondary roots (Fig. 1, B and C). In the leaves, expression was primarily limited to the hydathodes and more weakly to trichomes (Fig. 1D).
Following an initial observation of strong GUS expression at the cutting edge of a petiole in pH10::GUS plants (data not shown), expression of AtPHO1;H10 in wild-type plants treated with a variety of abiotic and biotic stresses was examined by RNA gel-blot analysis. In soil-grown plants, a strong accumulation of AtPHO1;H10 mRNA was observed in leaves 2 h after mechanical wounding, 2 h after initiation of dehydration, 12 h after cold treatment at 4°C, 4 h after paraquat treatment, 18 h after infection of leaves with Pseudomonas syringae pv. tomato DC3000 expressing or not the avirulence gene avrRpm1, and in senescing leaves (Fig. 1E). Similarly, a strong expression of AtPHO1;H10 in plants grown in agar-solidified medium was observed after 2 h of transfer to medium containing 100 mM NaCl or 4 h after transfer to 250 mM mannitol (Fig. 1E). Treatment of transgenic pH10::GUS plants with a subset of the stresses described above also showed strong GUS expression in either the roots (NaCl stress) or leaves (wounding, dehydration, senescence, and P. syringae infection [Fig. 1F]). However, no induction of AtPHO1;H10 expression could be detected by RNA gel-blot analysis in leaves following a heat shock at 37°C for 1 h (Fig. 1G). In pH10::GUS transgenic plants, GUS expression was restricted to the wound site for either leaves wounded mechanically with a razor blade, or challenged with the chewing caterpillar Pieris rapae (Fig. 2, B and D ). RNA gel-blot analysis confirmed that the up-regulation of AtPHO1;H10 expression in wounded or eaten leaves was restricted to the zone surrounding the wound site and not at a distal region in the same wounded leaves (Fig. 2, A and C).
AtPHO1;H10 Is Induced by ABA and OPDA But Not by JA or Coronatine The induction of AtPHO1;H10 following treatment of plants with various hormones and signal molecules involved in the response of plants to different biotic and abiotic stresses was examined by RNA gel-blot analysis. Treatment of plants with 100 µM ABA led to strong expression of AtPHO1;H10, with increased expression being detectable as early as 30 min after ABA addition and maximal expression observed at 2 h (Fig. 3A ). Strong expression of AtPHO1;H10 was also observed after 2 h of treatment with ABA concentrations ranging from 5 to 100 µM (Fig. 3B). Analysis of leaves 2, 4, and 8 h after infiltration with 1, 3, and 10 nmol of either JA or coronatine did not lead to the induction of AtPHO1;H10, whereas induction of the marker gene AtVSP2 was observed for JA and coronatine, respectively (Fig. 3, C and D). In contrast, infiltration of leaves with OPDA led to overexpression of AtPHO1;H10, with maximal expression observed after 3 h of infiltration with 3 nmol of OPDA (Fig. 3E). Infiltration of leaves of pH10::GUS plants with 3 nmol OPDA led to a local induction of GUS in the infiltrated area (Fig. 2E). No induction of AtPHO1;H10 expression was observed after 3 h of infiltration of leaves with 10 nmol oleic acid or linolenic acid (data not shown). Similarly, no induction of AtPHO1;H10 expression was observed in plants treated with methyl salicylate (Fig. 3F).
Induction of AtPHO1;H10 by Wounding Is Mediated by OPDA via a COI1-Dependent Pathway
Induction of AtPHO1;H10 by wounding was analyzed in various mutants affected in the jasmonate biosynthetic or perception pathway. The aos mutant is defective in the AOS gene, and is deficient in both OPDA and JA synthesis (Park et al., 2002 Overexpression of AtPHO1;H10 following mechanical wounding was nearly abolished in both the aos and coi1-1 mutant while it remained unaffected in the opr3 mutant (Fig. 4A ), indicating that endogenous OPDA synthesized following wounding was capable of inducing AtPHO1;H10 expression via a COI1-dependent pathway. Furthermore, induction of AtPHO1;H10 expression by infiltration of OPDA was also abolished in the coi1-1 mutant (Fig. 4B).
Wounding involves dehydration at the wound site and may involve an ABA-mediated response (Reymond et al., 2000 ). Induction of AtPHO;H10 following mechanical wounding was thus analyzed in the aba1-3 mutant deficient in ABA synthesis (Koornneef et al., 1982), and in the ABA-insensitive mutant abi1-1, deficient in multiple responses of plants to ABA (Koornneef et al., 1984). For both aba1-3 and abi1-1 mutants, the overexpression of AtPHO1;H10 following wounding was unchanged compared to the control (Fig. 4C).
The contribution of both the jasmonate- and ABA-mediated signaling pathway to the induction of AtPHO1;H10 expression following dehydration of rosette was assessed. Induction of AtPHO1;H10 was strongly reduced in both the aos and coi1-1 mutants, whereas only a slight reduction was observed in the opr3 mutant (Fig. 5A ). A strong reduction in AtPHO1;H10 expression following dehydration was also observed in the aba1-3 and abi1-1 mutant (Fig. 5B). Together, these results indicate a contribution of both OPDA and ABA to the response of AtPHO1;H10 to dehydration.
AtPHO1;H10 Expression by ABA Involves the ABI1 and ROP10 Signaling Pathway and Is Independent of the Jasmonate Pathway
Induction of AtPHO1;H10 expression by ABA in seedlings was strongly suppressed in abi1-1 (Fig. 6A
). ROP10 is a member of the ROP subfamily of Rho GTPases located in the plasma membrane and was shown to negatively regulate ABA-mediated responses (Zheng et al., 2002
Analysis of 1 kb of promoter sequence of AtPHO1;H10 revealed the sequences CACGTGTC and CACGTGGC 619 and 508 bp upstream of the start codon, respectively, which conforms to the cis-acting ABA responsive elements (ABREs). Furthermore, the sequence CACGCGT, which conforms to the CE3 coupling element, is found 23 bp upstream of the CACGTGGC ABRE (Rock, 2000 ). These sequences are recognized by members of the bZIP (basic-domain Leu zipper) transcription factors, which include ABF3, ABF4, and ABI5, three proteins involved in ABA-mediated responses (Rock, 2000; Yamaguchi-Shinozaki and Shinozaki, 2004). Expression of AtPHO1;H10 was analyzed in transgenic lines overexpressing the ABF3, ABF4, and ABI5 transcription factors under the control of the CaMV35S promoter (Kang et al., 2002; Lopez-Molina et al., 2002). In plants treated or untreated with ABA, overexpression of AtPHO1;H10 relative to wild-type plants was only observed in the ABI5-overexpressing lines (Fig. 6C). For the ABF3-overexpressing line, AtPHO1;H10 expression following ABA treatment was reduced compared to control (Fig. 6C). Finally, the overexpression of AtPHO1;H10 following ABA treatment was found to be unaffected in the aos and coi1-1 mutant (Fig. 6D).
The observed pattern of induction of AtPHO1;H10 expression by multiple stresses is largely in agreement with its induction by either exogenous ABA or OPDA applications. Changes in the endogenous level of ABA and the implication of the ABA signaling pathway has been well described for stresses mediated by wounding, dehydration, cold, senescence, salt, and osmotic stress (Pena-Cortes et al., 1989 , 1995; Birkenmeier and Ryan, 1998; Zhu, 2002; Gusta et al., 2005; de Torres-Zabala et al., 2007). ABA has also been implicated in the response of plants to pathogen infection, including infection with P. syringae (Anderson et al., 2004; Mauch-Mani and Mauch, 2005; Adie et al., 2007; de Torres-Zabala et al., 2007). Similarly, increase in endogenous level of OPDA and/or JA, as well as the implication of the JA signaling pathway has been described for wounding, dehydration, senescence, salt, osmotic, and oxidative stresses, as well as for infection with pathogens (Harms et al., 1995; Lehmann et al., 1995; Pena-Cortes et al., 1995; Herde et al., 1996; Moons et al., 1997; Reymond et al., 2000; Stinzi and Browse, 2000; He et al., 2002; Sasaki-Sekimoto et al., 2005; Truman et al., 2007). Thus, although it is not excluded that other molecules or signaling pathways could be involved in modulating the expression of AtPHO1;H10 in other stresses, these results reveal that both ABA and OPDA are important regulators for this gene.
Previous studies have shown that OPDA can have a biological activity that can either overlap with JA or be distinct from JA. Overlap in the activity of OPDA and JA has been shown by the maintenance of resistance to the dipteran B. impatiens and fungus A. brassicicola in the Arabidopsis mutant opr3, synthesizing OPDA but not JA (Stinzi et al., 2001
In accordance with the participation of JAZ proteins in the jasmonate signaling network, altered expression of some JAZ proteins lead to reduced sensitivity to JA (Chini et al., 2007 ; Thines et al., 2007; Yan et al., 2007). Physical interaction between COI1 and JAZ3/JAI3 or JAZ1 has been demonstrated in cell-free protein extracts, while interaction between JAZ1 and COI1 was further demonstrated in a yeast two-hybrid system (Chini et al., 2007; Thines et al., 2007). Remarkably, interaction between JAZ1 and COI1 was found to be dependent on the presence of JA-Ile, whereas OPDA, JA, or MeJA did not promote interactions between these proteins (Thines et al., 2007). Furthermore, proteasome degradation of JAZ3/JAI3 was impaired in the jar1 mutant deficient in the enzyme responsible for the synthesis of JA-Ile conjugate (Chini et al., 2007). Together, these results reveal that JA-Ile is an active hormone promoting the interaction between COI1 and either JAZ1 or JAZ3/JAI3. Furthermore, although OPDA was previously regarded as a close structural analog of coronatine (Weiler et al., 1994), the current data rather suggest that coronatine is a structural analog of JA-Ile (Staswick, 2008). In this context, what then is the significance of the activation of AtPHO1;H10 by OPDA and not JA or coronatine, in a COI1-dependent fashion? One hypothesis would be that OPDA promotes the interaction of COI1 with a distinct member of the JAZ protein family, which comprises 12 members in Arabidopsis. Alternatively, OPDA may activate AtPHO1;H10 through the interaction of COI1 with other unidentified proteins. The sets of genes regulated by COI1 would thus depend on both the nature of the jasmonate (e.g. OPDA or JA-Ile) and the presence of distinct effector molecules interacting with COI1. The distinct role of jasmonates other than JA-Ile has recently been supported by findings that wound-induced expression of COI1-dependent genes in the Arabidopsis JA-Ile-deficient jar1-1 mutant is not significantly impaired, and by the distinct role of JA and JA-Ile in herbivore resistance of Nicotiana attenuata (Wang et al., 2007; Chung et al., 2008).
Several physiological and developmental processes are influenced by either a synergistic or antagonistic cross talk between ABA and jasmonates, including seed germination (Wilen et al., 1991 Activation of AtPHO1;H10 expression by external ABA was independent of the presence of both AOS and COI1, but was strongly influenced by the presence of ABI1 and ROP10, indicating the lack of involvement of the jasmonate pathway and the main participation of the ABA signaling pathway in this activation. The presence of ABRE and C3 cis-acting elements in the promoter of AtPHO1;H10 and the activation of AtPHO1;H10 expression in the transgenic line overexpressing the ABI5 transcription factor further highlight the main contribution of the ABA signaling pathway via ABI5 in AtPHO1;H10 regulation. The lack of response of the AtPHO1;H10 gene to overexpression of ABF3 and ABF4 is in contrast to the strong activation of AtPHO1;H10 by ABI5 (Fig. 6B). These data likely reflect differential strength of interaction of these three transcription factors to the cis-promoter elements present in AtPHO1;H10.
The contribution of the ABA signaling pathway to AtPHO1;H10 expression following wounding and dehydration was distinct. Thus, AtPHO1;H10 induction by wounding was found to be unaffected in the aba1-3 and abi1-1 mutants, indicating that in contrast to the ABA-dependent activation of PIN2 in wounded potato and tomato leaves, induction of ATPHO1;H10 expression by wounding mainly involved the OPDA-COI1 pathway and was independent of the ABA pathway. In contrast, upon dehydration, both the ABA and OPDA-COI1 pathway needed to be present to achieve maximal AtPHO1;H10 expression. The implication of ABA upon dehydration could perhaps be linked to a higher increase in ABA level in dehydrated tissues compared to wounding (Creelman and Mullet, 1995
At present, the role of AtPHO1;H10 in the plant's response to wounding or water stress remains unclear. Although both AtPHO1 and its closest homolog AtPHO1;H1 are involved in the loading of inorganic phosphate to the xylem (Stefanovic et al., 2007
Plant Materials and Growth Conditions
Seeds of wild-type Arabidopsis (Arabidopsis thaliana) accession Columbia (Col), Landsberg erecta (Ler), or Wassilewskija (Ws), as well as of mutants (ecotypes of the mutants are indicated in parenthesis) aos (Col; Park et al., 2002
Wounding was done with incisions made with a razor blade across the whole surface at intervals of approximately 2 mm. The main vein and the edges of the leaf were left undamaged. Following wounding, plants were kept in the same growth room for 3 h before being harvested and frozen in liquid nitrogen. For biotic wounding experiments, Pieris rapae caterpillars were placed on plants and were allowed to feed under light for 5 h at 20°C until approximately 40% of the leaf surface was removed. Larvae were then removed, and all plant leaves were immediately frozen in liquid nitrogen or used for GUS assay. Dehydration was performed by excising the whole rosettes from their roots with a razor blade and then placing them on a paper in the same growth chamber at 20°C and 70% humidity for various times before freezing in liquid nitrogen. Stock solutions of 10 mM (±)-cis, trans-ABA (Sigma) was prepared in water with a few microliters of NaOH 1 N to help the dissolution. Solutions of 9S,13S-OPDA (Larodan), coronatine (Sigma), and the (±)-JA (Sigma) were infiltrated into the abaxial surface of the leaf with a syringe without a needle, at 10 µL per leaf. Before infiltration of OPDA, the ethanol was evaporated and the residues were dissolved in a volume of ethanol adjusted so that the final concentration of ethanol after water addition was 5% (v/v). To improve solubilization, OPDA solution was sonicated in a water bath. JA and coronatine were directly dissolved into water. Control leaves were infiltrated with water or water containing the same concentration of ethanol. Volatile methyl-salicylate (Sigma) treatments were done in hermetic plexiglass boxes (11.4 L) by applying either 7.9 µmol or 40 µmol of MeJA on a Q-tip (final concentration of 0.7 µmol or 3.5 µmol to 1 L of air volume, respectively). For infection of leaves with Pseudomonas syringae pv. tomato DC3000 with or without the avirulence gene avrRpm1, the abaxial surface of leaves was infiltrated with 2.5 x 105 colony-forming units in 10 µL of 10 mM MgCl2 using a syringe without a needle.
Total RNA was extracted from plants tissues by phenol:chloroform separation and lithium chloride precipitation followed by washes with sodium acetate and ethanol as previously described (Reymond et al., 2000
Transgenic plants expressing the uidA reporter gene under the control of a 1-kb fragment of the AtPHO1;H10 promoter (Wang et al., 2004
The authors thank Louis Lopez-Molina, Soo Young Kim, and Zhenbiao Yang for providing us with seeds for some of the mutants and transgenic lines used in this study, Caroline Darimont for her work on cDNA microarrays, and Pasqualina Magliano and Syndie Delessert for help with plant care. Received March 18, 2008; accepted April 8, 2008; published April 23, 2008.
1 This work was supported the Fonds National Suisse (grant no. 3100A0–105874 to Y.P.) and the Etat de Vaud. 
2 Present address: Bayer CropScience, 14–20 rue Pierre Baizet, 69263, Lyon cedex 9, France. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Yves Poirier (yves.poirier{at}unil.ch). www.plantphysiol.org/cgi/doi/10.1104/pp.108.119321 * Corresponding author; e-mail yves.poirier{at}unil.ch.
Adie BAT, Pérez-Pérez J, Pérez-Pérez MM, Godoy M, Sanchez-Serrano J, Schmelz EA, Solano R (2007) ABA is an essential signal for plant resistance of pathogens affecting JA biosynthesis and the activation of defenses in Arabidopsis. Plant Cell 19: 1665–1681 Anderson JP, Badruzsaufari E, Schenk PM, Manners JM, Desmond OJ, Ehlert C, Maclean DJ, Ebert PR, Kazan K (2004) Antagonistic interaction between abscisic acid and jasmonate-ethylene signaling pathways modulates defense gene expression and disease resistance in Arabidopsis. Plant Cell 16: 3460–3479 Birkenmeier GF, Ryan CA (1998) Wound signaling in tomato plants. Evidence that ABA is not a primary signal for defense gene action. Plant Physiol 117: 687–693 Blechert S, Bockelmann C, Füsslein M, Schrader TV, Stelmach B, Nielsen U, Weiler EW (1999) Structure-activity analyses reveal the existence of two separate groups of active octadecanoids in elicitation of the tendril-coiling response of Bryonia dioica Jacq. Planta 207: 470–479[CrossRef][Web of Science] Bodenhausen N, Reymond P (2007) Signaling pathways controlling induced resistance to insect herbivores in Arabidopsis. Mol Plant Microbe Interact 11: 1406–1420 Browse J, Howe GA (2008) New weapons and a rapid response against insect attack. Plant Physiol 146: 832–838 Carrera E, Prat S (1998) Expression of the Arabidopsis abi1-1 mutant allele inhibits proteinase inhibitor wound-induction in tomato. Plant J 15: 765–771[CrossRef][Web of Science][Medline] Chini A, Fonseca S, Fernandez G, Adie B, Chico JM, Lorenzo O, Garcia-Casado G, Lopez-Vidriero I, Lozano FM, Ponce MR, et al. (2007) The JAZ family of repressors is the missing link in jasmonate signalling. Nature 448: 666–671[CrossRef][Medline] Chung HS, Koo AJK, Gao X, Jayanty S, Thines B, Jones AD, Howe GA (2008) Regulation and function of Arabidopsis JASMONATE ZIM-domain genes in response to wounding and herbivory. Plant Physiol 146: 952–964 Creelman RA, Mullet JE (1995) Jasmonic acid distribution and action in plants: regulation during development and response to biotic and abiotic stress. Proc Natl Acad Sci USA 92: 4114–4119 Crowe ML, Serizet C, Thareau V, Aubourg S, Rouze P, Hilson P, Beynon J, Weisbeek P, van Hummelen P, Reymond P, et al. (2003) CATMA: a complete Arabidopsis GST database. Nucleic Acids Res 31: 156–158 Dammann C, Rojo E, Sanchez-Serrano J (1997) Abscisic acid and jasmonic acid activate wound-inducible genes in potato through separate, organ-specific signal transduction pathways. Plant J 11: 773–782[CrossRef][Web of Science][Medline] de Torres-Zabala M, Truman W, Bennett MH, Lafforgue G, Mansfiled JW, Egea PR, Bögre L, Grant M (2007) Pseudomonas syringae pv. tomato hijacks the Arabidopsis abscisic acid signalling pathway to cause disease. EMBO J 26: 1434–1443[CrossRef][Web of Science][Medline] Devoto A, Nieto-Rostro M, Xie D, Ellis C, Harmston R, Patrick E, Davis J, Sherratt L, Coleman M, Turner JG (2002) COI1 links jasmonate signalling and fertility to the SCF ubiquitin-ligase complex in Arabidopsis. Plant J 32: 457–466[CrossRef][Web of Science][Medline] Devoto A, Turner JG (2005) Jasmonate-regulated Arabidopsis stress signalling network. Physiol Plant 123: 161–172[CrossRef] Ellis C, Turner JG (2002) A conditionally fertile coi1 allele indicates cross-talk between plant hormone signalling pathways in Arabidopsis thaliana seeds and young seedlings. Planta 215: 549–556[CrossRef][Web of Science][Medline] Farmer EE, Alméras E, Krishnamurthy V (2003) Jasmonates and related oxylipins in plant responses to pathogenesis and herbivory. Curr Opin Plant Biol 6: 372–378[CrossRef][Web of Science][Medline] Feys BF, Benedetti CE, Penfold CN, Turner JG (1994) Arabidopsis mutants selected for resistance to the phytotoxin coronatine are male-sterile, insensitive to methyl jasmonate, and are resistant to a bacterial pathogen. Plant Cell 6: 751–759 Gusta LV, Trischuk R, Weiser CJ (2005) Plant cold acclimation: the role of abscisic acid. J Plant Growth Regul 24: 308–318[CrossRef][Web of Science] Hamburger D, Rezzonico E, MacDonald-Comber Petetot J, Somerville C, Poirier Y (2002) Identification and characterization of the Arabidopsis PHO1 gene involved in phosphate loading to the xylem. Plant Cell 14: 889–902 Harms K, Atzorn R, Brash A, Kühn H, Wasternack C, Willmitzer L, Pena-Cortes H (1995) Expression of a flax allene oxide synthase cDNA leads to increased endogenous jasmonic acid (JA) levels in transgenic plants but not to a corresponding activation of JA-responding genes. Plant Cell 7: 1645–1654[Abstract] He Y, Fukushige H, Hildebrand DF, Gan S (2002) Evidence supporting a role of jasmonic acid in Arabidopsis leaf senescence. Plant Physiol 128: 876–884 Herde O, Atzorn R, Fisahn J, Wasternack C, Willmitzer L, Pena-Cortes H (1996) Localized wounding by heat initiates the accumulation of proteinase inhibitor II in abscisic acid-deficient plants by triggering jasmonic acid biosynthesis. Plant Physiol 112: 853–860[Abstract] Hildmann T, Ebneth M, Pena-Cortes H, Sanchez-Serrano J, Willmitzer L, Prat S (1992) General roles of abscisic and jasmonic acids in gene activation as a result of mechanical wounding. Plant Cell 4: 1157–1170 Kang J-Y, Choi H-I, Inn M-Y, Kim SY (2002) Arabidopsis basic leucine zipper proteins that mediate stress-responsive abscisic acid signaling. Plant Cell 14: 343–357 Koornneef M, Jorna ML, Brinkhorst-van der Swan DLC, Karssen CM (1982) The isolation of abscisic acid (ABA) deficient mutants by selection of induced revertants in non-germinating gibberellin sensitive lines of Arabidopsis thaliana (L.) Heynh. Theor Appl Genet 61: 385–393[Web of Science] Koornneef M, Reuling G, Karssen CM (1984) The isolation and characterization of abscisic acid-insensitive mutants of Arabidopsis thaliana. Physiol Plant 61: 377–383[CrossRef] Kramell R, Miersch O, Atzorn R, Parthier B, Wasternack C (2000) Octadecanoid-derived alteration of gene expression and the "oxylipin signature" in stressed barley leaves. Implications for different signaling pathways. Plant Physiol 123: 177–187 Lee J, Parthier B, Löbler M (1996) Jasmonate signalling can be uncoupled from abscisic acid signalling in barley: identification of jasmonate-regulated transcripts which are not induced by abscisic acid. Planta 199: 625–632[Web of Science][Medline] Lehmann J, Atzorn R, Brückner C, Reinbothe S, Leopold J, Wasternack C, Parthier B (1995) Accumulation of jasmonate, abscisic acid, specific transcripts and proteins in osmotically stressed barley leaf segments. Planta 197: 156–162[Web of Science] Lopez-Molina L, Mongrand S, McLachlin DT, Chait BT, Chua NH (2002) ABI5 acts downstream of ABI3 to execute an ABA-dependent growth arrest during germination. Plant J 32: 317–328[CrossRef][Web of Science][Medline] Lorenzo O, Chico JM, Sanchez-Serrano J, Solano R (2004) JASMONATE-INSENSITIVE1 encodes a MYC transcription factor essential to discriminate between different jasmonate-regulated defense responses in Arabidopsis. Plant Cell 16: 1938–1950 Lorenzo O, Piqueras R, Sanchez-Serrano J, Solano R (2003) ETHYLENE RESPONSE FACTOR1 integrates signals from ethylene and jasmonate pathways in plant defense. Plant Cell 15: 165–178 Lorenzo O, Solano R (2005) Molecular players regulating the jasmonate signalling network. Curr Opin Plant Biol 8: 532–540[CrossRef][Web of Science][Medline] Mauch-Mani B, Mauch F (2005) The role of abscisic acid in plant-pathogen interactions. Curr Opin Plant Biol 8: 409–414[CrossRef][Web of Science][Medline] Moons A, Prinsen E, Bauw G, Van Montagu M (1997) Antagonistic effects of abscisic acid and jasmonates on salt stress-inducible transcripts in rice roots. Plant Cell 9: 2243–2259[Abstract] Mur LAJ, Kenton P, Atzorn R, Miersch O, Wasternack C (2006) The outcome of concentration-specific interactions between salicylate and jasmonate signaling include synergy, antagonism, and oxidative stress leading to cell death. Plant Physiol 140: 249–262 Ni M, Kang X (2006) Arabidopsis SHORT HYPOCOTYL UNDER BLUE1 contains SPX and EXS domains and acts in cryptochrome signaling. Plant Cell 18: 921–934 Park J-H, Halitschke R, Kim HB, Baldwin IT, Feldmann KA, Feyereisen R (2002) A knock-out mutation in allele oxide synthase results in male sterility and defective wound signal transduction in Arabidopsis due to a block in jasmonic acid biosynthesis. Plant J 31: 1–12[CrossRef][Web of Science][Medline] Pena-Cortes H, Fisahn J, Willmitzer L (1995) Signals involved in wound-induced proteinase inhibitor II gene expression in tomato and potato plants. Proc Natl Acad Sci USA 92: 4106–4113 Pena-Cortes H, Prat S, Atzorn R, Wasternack C, Willmitzer L (1996) Abscisic acid-deficient plants do not accumulate proteinase inhibitor II following systemin treatment. Planta 198: 447–451[CrossRef][Web of Science] Pena-Cortes H, Sanchez-Serrano J, Mertens R, Willmitzer L, Prat S (1989) Abscisic acid is involved in the wound-induced expression of the proteinase inhibitor II gene in potato and tomato. Proc Natl Acad Sci USA 86: 9851–9855 Poirier Y, Thoma S, Somerville C, Schiefelbein J (1991) A mutant of Arabidopsis deficient in xylem loading of phosphate. Plant Physiol 97: 1087–1093 Reymond P, Weber H, Damond M, Farmer EE (2000) Differential gene expression in response to mechanical wounding and insect feeding in Arabidopsis. Plant Cell 12: 707–719 Rock CD (2000) Pathways to abscisic acid-regulated gene expression. New Phytol 148: 357–396[CrossRef][Web of Science] Sanders PM, Lee PY, Biesgen C, Boone JD, Beals TP, Weiler EW, Goldberg RB (2000) The Arabidopsis DELAYED DEHISCENCE1 gene encodes an enzyme in the jasmonic acid synthesis pathway. Plant Cell 12: 1041–1061 Sasaki-Sekimoto Y, Taki N, Obayashi T, Aono M, Matsumoto F, Sakurai N, Suzuki H, Hirai MY, Noji M, Saito K, et al. (2005) Coordinated activation of metabolic pathways for antioxidants and defence compounds by jasmonates and their roles in stress tolerance in Arabidopsis. Plant J 44: 653–668[CrossRef][Web of Science][Medline] Schaller F, Schaller A, Stinzi A (2005) Biosynthesis and metabolism of jasmonates. J Plant Growth Regul 23: 179–199[Web of Science] Schilmiller AL, Howe GA (2005) Systemic signalling in the wound response. Curr Opin Plant Biol 8: 369–377[CrossRef][Web of Science][Medline] Staswick PE (2008) JAZing up jasmonate signaling. Trends Plant Sci 13: 66–71[CrossRef][Web of Science][Medline] Staswick PE, Su W, Howell SH (1992) Methyl jasmonate inhibition of root growth and induction of a leaf protein are decreased in an Arabidopsis thaliana mutant. Proc Natl Acad Sci USA 89: 6837–6840 Staswick PE, Tiryaki I (2004) The oxylipin signal jasmonic acid is activated by an enzyme that conjugates it to isoleucine in Arabidopsis. Plant Cell 16: 2117–2127 Stefanovic A, Ribot C, Rouached H, Wang Y, Chong J, Belbahri L, Delessert S, Poirier Y (2007) Members of the PHO1 gene family show limited functional redundancy in phosphate transfer to the shoot, and are regulated by phosphate deficiency via distinct pathways. Plant J 50: 982–994[CrossRef][Web of Science][Medline] Stelmach BA, Müller A, Hennig P, Laudert D, Andert L, Weiler EW (1998) Quantitation of the octadecanoid 12-oxo-phytodienoic acid, a signalling compound in mechanotransduction. Phytochemistry 47: 539–589[CrossRef][Web of Science][Medline] Stinzi A, Browse J (2000) The Arabidopsis male-sterile mutant, opr3, lacks the 12-oxophytodienoic acid reductase required for jasmonate synthesis. Proc Natl Acad Sci USA 97: 10625–10630 Stinzi A, Weber H, Reymond P, Browse J, Farmer EE (2001) Plant defense in the absence of jasmonic acid: the role of cyclopentenones. Proc Natl Acad Sci USA 98: 12837–12842 Taki N, Sasaki-Sekimoto Y, Obayashi T, Kikuta A, Kobayashi K, Ainai T, Yagi K, Sakurai N, Suzuki H, Masuda T, et al (2005) 12-Oxo-phytodienoic acid triggers expression of a distinct set of genes and plays a role in wound-induced gene expression in Arabidopsis. Plant Physiol 139: 1268–1283 Thines B, Katsir L, Melotto M, Niu Y, Mandaokar A, Liu G, Nomura K, He SY, Howe GA, Browse J (2007) JAZ repressor proteins are targets of the SCFCOI1 complex during jasmonate signaling. Nature 448: 661–665[CrossRef][Medline] Truman W, Bennett MH, Kubigsteltig I, Turnbull C, Grant M (2007) Arabidopsis systemic immunity uses conserved defense signaling pathways and is mediated by jasmonates. Proc Natl Acad Sci USA 104: 1075–1080 Wang L, Allmann S, Wu J, Baldwin IT (2007) Comparisons of LIPOXYGENASE3- and JASMONATE RESISTANT4/6-silenced plants reveal that jasmonic acid and jasmonic acid-amino acid conjugates play different roles in herbivore resistance of Nicotiana attenuata. Plant Physiol 146: 904–915[Web of Science][Medline] Wang Y, Ribot C, Rezzonico E, Poirier Y (2004) Structure and expression profile of the Arabidopsis PHO1 gene family indicates a broad role in inorganic phosphate homeostasis. Plant Physiol 135: 400–411 Wasternack C (2007) Jasmonates: an update on biosynthesis, signal transduction and action in plant stress response, growth and development. Ann Bot (Lond) 100: 681–697 Weiler EW, Kutchan TM, Gorba T, Brodschelm W, Niesel U, Bublitz F (1994) The Pseudomonas phytotoxin coronatine mimics octadecanoid signalling molecules of higher plants. FEBS Lett 345: 9–13[CrossRef][Web of Science][Medline] Wilen RW, van Rooijen GJH, Pearce DW, Pharis RP, Holbrook LA, Moloney MM (1991) Effects of jasmonic acid on embryo-specific processes in Brassica and Linum oilseed. Plant Physiol 95: 399–405 Xie DX, Feys BF, James S, Nieto-Rostro M, Turner JG (1998) COI1: an Arabidopsis gene required for jasmonate-regulated defense and fertility. Science 280: 1091–1094 Xu L, Liu F, Wang Z, Peng W, Huang R, Huang D, Xie D (2001) The SCF(COI1) ubiquitin-ligase complexes are required for jasmonate response in Arabidopsis. Plant Cell 14: 1919–1935[Web of Science] Yamaguchi-Shinozaki K, Shinozaki K (2004) Organization of cis-acting regulatory elements in osmotic- and cold-stress-responsive promoters. Trends Plant Sci 10: 88–94[CrossRef][Web of Science] Yan Y, Stolz S, Chételat A, Reymond P, Pagni P, Dubugnon L, Farmer EE (2007) A downstream mediator in the growth repression limb of the jasmonate pathway. Plant Cell 19: 1–13 Zheng ZL, Nafisi M, Tam A, Li H, Crowell DN, Chary SN, Schroeder JI, Shen J, Yang Z (2002) Plasma membrane-associated ROP10 small GTPase is a specific negative regulator of abscisic acid responses in Arabidopsis. Plant Cell 14: 2787–2797 Zhu J-K (2002) Salt and drought stress signal transduction in plants. Annu Rev Plant Physiol Plant Mol Biol 53: 247–273[CrossRef][Medline] This article has been cited by other articles:
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-linolenic acid to 13-hydroperoxylinolenic acid (Schaller et al., 2005
