FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022081062> ?p ?o ?g. }

• W2022081062 endingPage "257" @default.
• W2022081062 startingPage "249" @default.
• W2022081062 abstract "Plants have sophisticated defense systems to protect their tissues against the attack of herbivorous organisms. Many of these defenses are orchestrated by the oxylipin jasmonate. A growing body of evidence indicates that the expression of jasmonate-induced responses is tightly regulated by the ecological context of the plant. Ecological information is provided by molecular signals that indicate the nature of the attacker, the value of the attacked organs, phytochrome status and thereby proximity of competing plants, association with beneficial organisms and history of plant interactions with pathogens and herbivores. This review discusses recent advances in this field and highlights the need to map the activities of informational modulators to specific control points within our emerging model of jasmonate signaling. Plants have sophisticated defense systems to protect their tissues against the attack of herbivorous organisms. Many of these defenses are orchestrated by the oxylipin jasmonate. A growing body of evidence indicates that the expression of jasmonate-induced responses is tightly regulated by the ecological context of the plant. Ecological information is provided by molecular signals that indicate the nature of the attacker, the value of the attacked organs, phytochrome status and thereby proximity of competing plants, association with beneficial organisms and history of plant interactions with pathogens and herbivores. This review discusses recent advances in this field and highlights the need to map the activities of informational modulators to specific control points within our emerging model of jasmonate signaling. Jasmonate (JA) signalingJA is an oxylipin involved in the regulation of several physiological processes [1Browse J. Jasmonate passes muster: a receptor and targets for the defense hormone.Annu. Rev. Plant Biol. 2009; 60: 183-205Crossref PubMed Scopus (224) Google Scholar]. JAs were first connected with defense responses by the work of E.E. Farmer and C.A. Ryan [2Farmer E.E. Ryan C.A. Interplant communication: airborne methyl jasmonate induces synthesis of proteinase inhibitors in plant leaves.Proc. Natl. Acad. Sci. U.S.A. 1990; 87: 7713-7716Crossref PubMed Scopus (1034) Google Scholar, 3Farmer E.E. Ryan C.A. Octadecanoid precursors of jasmonic acid activate the synthesis of wound-inducible proteinase inhibitors.Plant Cell. 1992; 4: 129-134PubMed Google Scholar] on the regulation of the expression of digestive proteinase inhibitors in the tomato (Solanum lycopersicum). Two decades after that exciting discovery, it is now firmly established that JA is a key cellular signal involved in the activation of immune responses to most insect herbivores and necrotrophic microorganisms (see Box 1 for defense-related terminology). The early signaling steps involved in the perception of the attack by herbivores or pathogens, through the detection of herbivore- and damage-associated molecular patterns (HAMPs and DAMPs, respectively) [4Felton G.W. Tumlinson J.H. Plant-insect dialogs: complex interactions at the plant-insect interface.Curr. Opin. Plant Biol. 2008; 11: 457-463Crossref PubMed Scopus (62) Google Scholar], and the activation of JA biosynthesis remain to be elucidated [5Howe G.A. Jander G. Plant immunity to insect herbivores.Annu. Rev. Plant Biol. 2008; 59: 41-66Crossref PubMed Scopus (455) Google Scholar]. However, the details of the mechanism used by plant cells to perceive elevated levels of bioactive JA and transduce the JA signal into the activation of transcriptional responses have been thoroughly investigated in the past few years. Recent work has also demonstrated that JA signaling is finely controlled by internal and external signals that provide the plant with information about its physiological status and ecological context. Therefore, an emerging major challenge is to find the functional links between these ecological regulators and the key molecular players involved in the control of JA responses. Whereas recent reviews have covered particular aspects of the regulation of JA responses, including crosstalk with other hormones [6Kazan K. Manners J.M. Jasmonate signaling: toward an integrated view.Plant Physiol. 2008; 146: 1459-1468Crossref PubMed Scopus (119) Google Scholar, 7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 8Verhage A. et al.Plant immunity: it's the hormones talking, but what do they say?.Plant Physiol. 2010; 154: 536-540Crossref PubMed Scopus (64) Google Scholar] and modulation by light signals [9Ballaré C.L. Illuminated behaviour: phytochrome as a key regulator of light foraging and plant anti-herbivore defence.Plant Cell Environ. 2009; 32: 713-725Crossref PubMed Scopus (64) Google Scholar], we still lack an integrated picture of plausible interactions among ecological regulators and the connections between these regulators and the recently discovered molecular components of the JA response.Box 1Basic glossary for plant enemies and defensesPlant enemiesPlants are targeted by a wide spectrum of consumer organisms, which include pathogens (such as viruses, bacteria, fungi and oomycetes) and pests (such as herbivorous insects and nematodes). Plant pathogens are generally divided into biotrophs and necrotrophs according to their lifestyles [108Glazebrook J. Contrasting mechanisms of defense against biotrophic and necrotrophic pathogens.Annu. Rev. Phytopathol. 2005; 43: 205-227Crossref PubMed Scopus (974) Google Scholar]. Biotrophs derive their nutrients from living plant tissue, frequently by using haustoria that penetrate the plant cells without causing extensive cell damage. Necrotrophs first kill the host cells, often through the production of specialized toxins, and then feed on the remains. Some plant pathogens can display both lifestyles (e.g. depending on the stage of their life cycle), and are termed hemibiotrophs. Herbivorous insects are frequently divided according to their feeding styles into biting–chewing insects (which bite off and chew their food) or sucking insects (which pierce the plant tissue using specialized mouth parts and absorb liquid cell contents) [109Schoonhoven L.M. et al.Insect-Plant Biology. Oxford University Press, 2005Google Scholar].Constitutive and induced defensesPlants have several lines of constitutive (i.e. preformed) structural and chemical defenses to prevent attacks from a diverse array of enemies. If these initial layers of defense are broken, plants rely on a complex and highly regulated system of inducible responses (i.e. responses that are activated only when the plant is under attack by pathogens or herbivores). The expression of these induced defenses is coordinated by defense-related hormones.Defense-related hormones (JA, SA and ET)In addition to JA, which coordinates the defense responses against chewing insects (often termed the ‘wound’ response) and necrotrophic pathogens, two other hormones play key roles in orchestrating the expression of the plant immune system: SA and ET [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 108Glazebrook J. Contrasting mechanisms of defense against biotrophic and necrotrophic pathogens.Annu. Rev. Phytopathol. 2005; 43: 205-227Crossref PubMed Scopus (974) Google Scholar]. The SA response pathway is activated by plants in response to attack by pathogens with biotrophic lifestyles [108Glazebrook J. Contrasting mechanisms of defense against biotrophic and necrotrophic pathogens.Annu. Rev. Phytopathol. 2005; 43: 205-227Crossref PubMed Scopus (974) Google Scholar]. The plant defense response is initiated upon the recognition of pathogen signatures (PAMPS and microbial effector proteins) and often involves an increase in the levels of SA, programmed cell death at the site of infection and the accumulation of antimicrobial metabolites in systemic tissues (including PR proteins). The accumulation of defenses in tissues distal from the site of infection is called systemic-acquired resistance (SAR) and this confers broad-spectrum, long-lasting resistance against microbial pathogens. ET is a gaseous plant hormone whose production is frequently induced in response to attack by necrotrophic pathogens and some types of herbivore insects, as well by several stressors and environmental and developmental signals. ET plays an important role as a modulator of SA and JA responses [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 25Bostock R.M. Signal crosstalk and induced resistance: straddling the line between cost and benefit.Annu. Rev. Phytopathol. 2005; 43: 545-580Crossref PubMed Scopus (247) Google Scholar, 43von Dahl C. Baldwin I. Deciphering the role of ethylene in plant–herbivore interactions.J. Plant Growth Reg. 2007; 26: 201-209Crossref Scopus (59) Google Scholar].In this review, I will focus on this active area of research and attempt to generate a preliminary map of the signaling circuits that modulate JA-induced defenses as a function of physiological signals and plant interactions with a diverse array of ecological actors, including consumers, competitors and beneficial organisms.JA perceptionThe core events of JA perception (Figure 1) have recently been identified [10Chini A. et al.The JAZ family of repressors is the missing link in jasmonate signalling.Nature. 2007; 448: 666-671Crossref PubMed Scopus (524) Google Scholar, 11Thines B. et al.JAZ repressor proteins are targets of the SCFCOI1 complex during jasmonate signalling.Nature. 2007; 448: 661-665Crossref PubMed Scopus (568) Google Scholar, 12Yan Y. et al.A downstream mediator in the growth repression limb of the jasmonate pathway.Plant Cell. 2007; 19: 2470-2483Crossref PubMed Scopus (168) Google Scholar, 13Melotto M. et al.A critical role of two positively charged amino acids in the Jas motif of Arabidopsis JAZ proteins in mediating coronatine- and jasmonoyl isoleucine-dependent interactions with the COI1 F-box protein.Plant J. 2008; 55: 979-988Crossref PubMed Scopus (89) Google Scholar, 14Yan J.B. et al.The Arabidopsis CORONATINE INSENSITIVE1 protein is a jasmonate receptor.Plant Cell. 2009; 21: 2220-2236Crossref PubMed Scopus (183) Google Scholar, 15Pauwels L. et al.NINJA connects the co-repressor TOPLESS to jasmonate signalling.Nature. 2010; 464: 788-791Crossref PubMed Scopus (140) Google Scholar, 16Sheard L.B. et al.Jasmonate perception by inositol-phosphate-potentiated COI1-JAZ co-receptor.Nature. 2010; 468: 400-407Crossref PubMed Scopus (169) Google Scholar] and are discussed in several review papers [1Browse J. Jasmonate passes muster: a receptor and targets for the defense hormone.Annu. Rev. Plant Biol. 2009; 60: 183-205Crossref PubMed Scopus (224) Google Scholar, 17Fonseca S. et al.The jasmonate pathway: the ligand, the receptor and the core signalling module.Curr. Opin. Plant Biol. 2009; 12: 539-547Crossref PubMed Scopus (73) Google Scholar, 18Chung H.S. et al.Top hits in contemporary JAZ: an update on jasmonate signaling.Phytochem. 2009; 70: 1547-1559Crossref PubMed Scopus (50) Google Scholar, 19Howe G.A. Ubiquitin ligase-coupled receptors extend their reach to jasmonate.Plant Physiol. 2010; 154: 471-474Crossref PubMed Scopus (11) Google Scholar]. Briefly, the perception of jasmonoyl-isoleucine (JA-Ile), the bioactive amino acid conjugate of jasmonic acid, is achieved by the ubiquitin ligase SCFCOI1 complex. When the F-box protein CORONATINE-INSENSITIVE1 (COI1) recognizes JA-Ile, it triggers the ubiquitination and subsequent proteosomal degradation of JASMONATE ZIM DOMAIN (JAZ) proteins. The degradation of JAZ proteins relieves JAZ-mediated repression of gene expression, leading to the activation of JA responses (Figure 1). Recent structural and pharmacological studies [16Sheard L.B. et al.Jasmonate perception by inositol-phosphate-potentiated COI1-JAZ co-receptor.Nature. 2010; 468: 400-407Crossref PubMed Scopus (169) Google Scholar] have indicated that the complex of both COI1 and JAZ (Figure 1) should be considered the true JA-Ile receptor. This is because COI1 contains an open pocket that recognizes JA-Ile, but a loop region in the JAZ protein is necessary to trap the hormone in this binding pocket; furthermore, these studies identified a third crucial component of the JA coreceptor complex, inositol pentakisphosphate, which interacts with both COI1 and JAZ adjacent to the ligand [16Sheard L.B. et al.Jasmonate perception by inositol-phosphate-potentiated COI1-JAZ co-receptor.Nature. 2010; 468: 400-407Crossref PubMed Scopus (169) Google Scholar]. The activation of JA-responsive genes leads to the production of metabolites involved in defense. In addition, the local activation of the JA signaling cascade produces signaling molecules that propagate systemically to induce JA responses in organs not directly affected by the initial event of herbivory or pathogen infection, and provide protection against future attacks [5Howe G.A. Jander G. Plant immunity to insect herbivores.Annu. Rev. Plant Biol. 2008; 59: 41-66Crossref PubMed Scopus (455) Google Scholar, 20Koo A.J.K. et al.A rapid wound signal activates the systemic synthesis of bioactive jasmonates in Arabidopsis.Plant J. 2009; 59: 974-986Crossref PubMed Scopus (86) Google Scholar].Adaptive modulationOne of the key aspects of the plant defense response is that its expression is modulated by the ecological context of the plant. Thus, the timing, intensity and characteristics of the defense repertoire are influenced by the specific nature of the attacker, the vitality of the attacked organs, the proximity of competing plants, the association with beneficial organisms and the history of previous interactions with pathogens and herbivores. This regulation of plant defense is a clear example of the role played by information-acquiring systems in tailoring adaptive plant behavior [9Ballaré C.L. Illuminated behaviour: phytochrome as a key regulator of light foraging and plant anti-herbivore defence.Plant Cell Environ. 2009; 32: 713-725Crossref PubMed Scopus (64) Google Scholar, 21Karban R. Plant behaviour and communication.Ecol. Lett. 2008; 11: 727-739Crossref PubMed Scopus (73) Google Scholar, 22Trewavas A. What is plant behaviour?.Plant Cell Environ. 2009; 32: 606-616Crossref PubMed Scopus (35) Google Scholar].Recent work has suggested that the plastic regulation of plant defense expression is achieved, at least in part, through the intricate, multilayer modulation of the JA signaling pathway. Our understanding of this modulation by environmental and internal signals, which is outlined in Figure 2, is still limited. In the following sections, I will discuss some of the key features and regulators of JA responses that contribute to the adaptive adjustment of the defense strategy of the plant.Figure 2The modulation of the JA response by internal and external signals. The perception of HAMPs and DAMPs when plants are under attack by herbivores and necrotrophs activates the JA biosynthetic pathway. The production of bioactive JA-Ile leads to the derepression of the relevant transcription factors and defense-related genes, and the activation of plant defenses. The expression of the JA response is modulated by several physiological and ecological signals. The proximity of competing plants increases the levels of FR radiation, which weakens JA responses by converting the active, Pfr form of phyB (a positive regulator of JA sensitivity) into the inactive Pr form. Attacks from pathogens with a biotrophic lifestyle activate the SA pathway, which generally antagonizes the JA response. The SA effect is modulated by ET, which is another hormone frequently induced by the plant in response to HAMPs and DAMPs. Plant association with beneficial microorganisms can increase the JA response, presumably by increasing the abundance of defense-related transcription factors. The levels of several additional hormones contain information on the internal status of the plant tissue to be defended, and also regulate JA responses. BR and GA (two growth-promoting hormones) repress JA responses; this interaction might play a role in regulating the growth vs. defense allocation tradeoff. CK is a positive regulator of the JA response. CK concentrations are typically low in shaded and old leaves, and along with Pfr levels CKs might help concentrate the defense response in the most photosynthetically active (valuable) leaf elements. Defense responses are also potentiated by volatile signals (such as GLVs) produced by herbivore-attacked neighboring leaves. Arrows indicate promotion/activation; truncated lines indicate repression or negative interactions. For some regulators, the precise point of interaction with the JA signaling pathway is unknown, which is indicated by the dotted green line at the site of convergence. BR, brassinosteroid; CK, cytokinin; ET, ethylene; GA, gibberellin; GLV, green leaf volatiles; SA, salicylate; TF, transcription factor.View Large Image Figure ViewerDownload (PPT)Intelligent focusing: choosing the defense strategyThe activation of plant defenses implies allocation and ecological costs [23Cipollini D. Stretching the limits of plasticity: can a plant defend against both competitors and herbivores?.Ecology. 2004; 85: 28-37Crossref Google Scholar, 24Baldwin I.T. An ecologically motivated analysis of plant-herbivore interactions in native tobacco.Plant Physiol. 2001; 127: 1449-1458Crossref PubMed Google Scholar, 25Bostock R.M. Signal crosstalk and induced resistance: straddling the line between cost and benefit.Annu. Rev. Phytopathol. 2005; 43: 545-580Crossref PubMed Scopus (247) Google Scholar, 26Cipollini D. Constitutive expression of methyl jasmonate-inducible responses delays reproduction and constrains fitness responses to nutrients in Arabidopsis thaliana.Evol. Ecol. 2010; 24: 59-68Crossref Scopus (10) Google Scholar, 27Heil M. Karban R. Explaining evolution of plant communication by airborne signals.Trends Ecol. Evol. 2010; 25: 137-144Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar]. For example, the allocation of resources to defense against one type of attacker can reduce the ability of the plant to respond to the challenge of a different invader. Plants seem to use mechanisms that effectively adjust their defense repertoires on the basis of the characteristics of their attackers. These mechanisms of ‘intelligent focusing’ are frequently mediated by hormonal crosstalk [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 8Verhage A. et al.Plant immunity: it's the hormones talking, but what do they say?.Plant Physiol. 2010; 154: 536-540Crossref PubMed Scopus (64) Google Scholar, 25Bostock R.M. Signal crosstalk and induced resistance: straddling the line between cost and benefit.Annu. Rev. Phytopathol. 2005; 43: 545-580Crossref PubMed Scopus (247) Google Scholar, 28Kunkel B.N. Brooks D.M. Cross talk between signaling pathways in pathogen defense.Curr. Opin. Plant Biol. 2002; 5: 325-331Crossref PubMed Scopus (582) Google Scholar, 29Koornneef A. Pieterse C.M.J. Cross talk in defense signaling.Plant Physiol. 2008; 146: 839-844Crossref PubMed Scopus (244) Google Scholar, 30Spoel S.H. Dong X. Making sense of hormone crosstalk during plant immune responses.Cell Host Microb. 2008; 3: 348-351Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar].A thoroughly characterized case of signal crosstalk is the antagonistic interaction between the JA and salicylic acid (SA) signaling pathways [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 25Bostock R.M. Signal crosstalk and induced resistance: straddling the line between cost and benefit.Annu. Rev. Phytopathol. 2005; 43: 545-580Crossref PubMed Scopus (247) Google Scholar, 28Kunkel B.N. Brooks D.M. Cross talk between signaling pathways in pathogen defense.Curr. Opin. Plant Biol. 2002; 5: 325-331Crossref PubMed Scopus (582) Google Scholar]. Plants infected by SA-inducing biotrophic pathogens often suppress JA-dependent defenses [31Felton G.W. Korth K.L. Trade-offs between pathogen and herbivore resistance.Curr. Opin. Plant Biol. 2000; 3: 309-314Crossref PubMed Scopus (139) Google Scholar, 32Spoel S.H. et al.Regulation of tradeoffs between plant defenses against pathogens with different lifestyles.Proc. Natl. Acad. Sci. U.S.A. 2007; 104: 18842-18847Crossref PubMed Scopus (156) Google Scholar], apparently prioritizing the investment of resources in SA-dependent defense over JA-dependent responses (Figure 2). Similarly, the elicitation of the JA pathway can repress the SA response [33Brooks D.M. et al.The Pseudomonas syringae phytotoxin coronatine promotes virulence by overcoming salicylic acid-dependent defences in Arabidopsis thaliana.Mol. Plant Pathol. 2005; 6: 629-639Crossref PubMed Scopus (109) Google Scholar, 34Uppalapati S.R. et al.The phytotoxin coronatine contributes to pathogen fitness and is required for suppression of salicylic acid accumulation in tomato inoculated with Pseudomonas syringae pv. tomato DC3000.Mol. Plant-Microbe Interac. 2007; 20: 955-965Crossref PubMed Scopus (70) Google Scholar].The mechanisms whereby SA modulates the JA response have been the subject of intense investigations and are discussed in several recent reviews [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 8Verhage A. et al.Plant immunity: it's the hormones talking, but what do they say?.Plant Physiol. 2010; 154: 536-540Crossref PubMed Scopus (64) Google Scholar, 29Koornneef A. Pieterse C.M.J. Cross talk in defense signaling.Plant Physiol. 2008; 146: 839-844Crossref PubMed Scopus (244) Google Scholar]. Briefly, SA can depress both JA biosynthesis and sensitivity [35Spoel S.H. et al.NPR1 modulates cross-talk between salicylate- and jasmonate-dependent defense pathways through a novel function in the cytosol.Plant Cell. 2003; 15: 760-770Crossref PubMed Scopus (403) Google Scholar]. The downregulation of JA biosynthesis is thought to be a byproduct of the reduced JA sensitivity, because several JA biosynthetic genes are positively regulated by JA, and it does not seem to be required for the SA-mediated suppression of JA signaling [36Leon-Reyes A. et al.Salicylate-mediated suppression of jasmonate-responsive gene expression in Arabidopsis is targeted downstream of the jasmonate biosynthesis pathway.Planta. 2010; 232: 1423-1432Crossref PubMed Scopus (47) Google Scholar]. The protein NPR1 (for NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1) plays an important role in mediating the suppressive effects of SA downstream of JA. NPR1 is a crucial component of SA signaling, which is activated by SA-induced redox changes that reduce inactive NPR1 oligomers to active monomers. NPR1 monomers are translocated to the nucleus, where they function as coactivators of TGA transcription factors that regulate the expression of SA-responsive genes, including PR genes [37Dong X. NPR1, all things considered.Curr. Opin. Plant Biol. 2004; 7: 547-552Crossref PubMed Scopus (278) Google Scholar]. The role of NPR1 in the repression of JA responses has been investigated by elegant experiments carried out in Arabidopsis (Arabidopsis thaliana), which were inspired by the structural analogies between NPR1 and IkB [35Spoel S.H. et al.NPR1 modulates cross-talk between salicylate- and jasmonate-dependent defense pathways through a novel function in the cytosol.Plant Cell. 2003; 15: 760-770Crossref PubMed Scopus (403) Google Scholar]. IkB is a protein that plays a key role in regulating the effects of SA and aspirin as suppressors of the formation of prostaglandins, which are animal oxylipins involved in inflammatory responses to infection and tissue damage. Those experiments demonstrated that NPR1 is required for the suppressive effects of SA on pathogen-induced JA accumulation and JA-induced defense gene expression. However, nuclear localization was not required for the suppression of JA signaling, indicating that the effects of SA on JA signaling are mediated through the activity of NPR1 in the cytosol [35Spoel S.H. et al.NPR1 modulates cross-talk between salicylate- and jasmonate-dependent defense pathways through a novel function in the cytosol.Plant Cell. 2003; 15: 760-770Crossref PubMed Scopus (403) Google Scholar, 38Glazebrook J. et al.Topology of the network integrating salicylate and jasmonate signal transduction derived from global expression phenotyping.Plant J. 2003; 34: 217-228Crossref PubMed Scopus (272) Google Scholar].The molecular mechanisms that mediate the effects of NPR1 suppressing JA-dependent defenses remain to be identified [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 30Spoel S.H. Dong X. Making sense of hormone crosstalk during plant immune responses.Cell Host Microb. 2008; 3: 348-351Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar]. Pharmacological and mutant studies in Arabidopsis have suggested that the NPR1-dependent effect of SA on JA signaling occurs downstream of the initial events of JA perception by the SCFCOI1 complex and JAZ degradation (Figure 1), and probably targets the GCC box in JA-responsive genes [39Leon-Reyes, A. (2009) Making sense out of signaling during plant defense. Doctoral Thesis. Utrecht UniversityGoogle Scholar]. The GCC box is a binding site for the transcription factors of the APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) superfamily that regulate the JA-induced response of several genes involved in plant defense, such as the plant defensin PDF1.2. NPR1-independent negative effects of SA on JA signaling have been reported [39Leon-Reyes, A. (2009) Making sense out of signaling during plant defense. Doctoral Thesis. Utrecht UniversityGoogle Scholar, 40Bruessow F. et al.Insect eggs suppress plant defence against chewing herbivores.Plant J. 2010; 62: 876-885Crossref PubMed Scopus (36) Google Scholar], and recent studies have also shown that ethylene (ET) can bypass the requirement for NPR1 in the SA-induced depression of JA response [41Leon-Reyes A. et al.Ethylene modulates the role of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 in cross talk between salicylate and jasmonate signaling.Plant Physiol. 2009; 149: 1797-1809Crossref PubMed Scopus (93) Google Scholar]. In Nicotiana attenuata plants exposed to herbivore attack, NPR1 downregulates SA production; this has been interpreted as a strategy evolved by the plant to prevent the depression of JA-induced defenses by herbivores that activate the SA pathway (see ‘The rascals’) [42Rayapuram C. Baldwin I.T. Increased SA in NPR1-silenced plants antagonizes JA and JA-dependent direct and indirect defenses in herbivore-attacked Nicotiana attenuata in nature.Plant J. 2007; 52: 700-715Crossref PubMed Scopus (52) Google Scholar].ET is another important modulator of JA-induced defense responses [7Pieterse C.M.J. et al.Networking by small-molecule hormones in plant immunity.Nat. Chem. Biol. 2009; 5: 308-316Crossref PubMed Scopus (353) Google Scholar, 25Bostock R.M. Signal crosstalk and induced resistance: straddling the line between cost and benefit.Annu. Rev. Phytopathol. 2005; 43: 545-580Crossref PubMed Scopus (247) Google Scholar, 43von Dahl C. Baldwin I. Deciphering the role of ethylene in plant–herbivore interactions.J. Plant Growth Reg. 2007; 26: 201-209Crossref Scopus (59) Google Scholar] (Figure 2). ET and JA frequently show a synergistic interaction in the induction of certain plant defenses, such as the upregulation of PDF1.2 in Arabidopsis [44Penninckx I.A.M.A. et al.Concomitant activation of Jasmonate and ethylene response pathways is required for induction of a plant defensin gene in Arabidopsis.Plant Cell. 1998; 10: 2103-2114PubMed Google Scholar]. The synergistic effect between JA and ET has been attributed to the concomitant activation of common transcription factors, such as those that belong to the AP2/ERF superfamily in Arabidopsis [45Lorenzo O. et al.ETHYLENE RESPONSE FACTOR1 integrates signals from ethylene and jasmonate pathways in plant defense.Plant Cell. 2003; 15: 165-178Crossref PubMed Scopus (426) Google Scholar, 46Pre M. et al.The AP2/ERF domain transcription factor ORA59 integrates jasmonic acid and ethylene signals in plant defense.Plant Physiol. 2008; 147: 1347-1357Crossref PubMed Scopus (138) Google Scholar] and the HD-Zip HAHB4 in the sunflower (Helianthus annuus) [47Manavella P.A. et al.HAHB4, a sunflower HD-Zip protein, integrates signals from the jasmonic acid and ethylene pathways during wounding and biotic stress responses.Plant J. 2008; 56: 376-388Crossref PubMed Scopus (16) Google Scholar]. However, cases of negative interactions (ET inhibiting JA-induced responses) have also been reported [48Winz R.A. Baldwin I.T. Molecular interactions between the specialist herbivore Manduca sexta (Lepidoptera, Sphingidae) and its natural host Nicotiana attenuata. IV. Insect-induced ethylene reduces jasmonate-induced nicotine accumulation by regulating putrescine N-methyltransferase transcripts.Plant Physiol. 2001; 125: 2189-2202Crossref PubMed Scopus (140) Google Scholar]. In addition, ET can cancel the effect of SA as a downregulator of JA responses. For example, a recent study has shown that the activation of the ET pathway renders the plant insensitive to the suppressive effects of SA on JA-induced defense" @default.
• W2022081062 created "2016-06-24" @default.
• W2022081062 creator A5052381433 @default.
• W2022081062 date "2011-05-01" @default.
• W2022081062 modified "2023-10-16" @default.
• W2022081062 title "Jasmonate-induced defenses: a tale of intelligence, collaborators and rascals" @default.
• W2022081062 cites W1492663715 @default.
• W2022081062 cites W1964741545 @default.
• W2022081062 cites W1971243790 @default.
• W2022081062 cites W1978073607 @default.
• W2022081062 cites W1979066476 @default.
• W2022081062 cites W1979740371 @default.
• W2022081062 cites W1980814578 @default.
• W2022081062 cites W1983239832 @default.
• W2022081062 cites W1985298763 @default.
• W2022081062 cites W1990151103 @default.
• W2022081062 cites W1990806343 @default.
• W2022081062 cites W1992031820 @default.
• W2022081062 cites W1994152184 @default.
• W2022081062 cites W1998336780 @default.
• W2022081062 cites W1999062682 @default.
• W2022081062 cites W2002242173 @default.
• W2022081062 cites W2007383318 @default.
• W2022081062 cites W2007689499 @default.
• W2022081062 cites W2011130378 @default.
• W2022081062 cites W2012747583 @default.
• W2022081062 cites W2013602706 @default.
• W2022081062 cites W2019344037 @default.
• W2022081062 cites W2019797603 @default.
• W2022081062 cites W2020674011 @default.
• W2022081062 cites W2024653949 @default.
• W2022081062 cites W2029058641 @default.
• W2022081062 cites W2030001397 @default.
• W2022081062 cites W2034436996 @default.
• W2022081062 cites W2035649408 @default.
• W2022081062 cites W2036165278 @default.
• W2022081062 cites W2037115380 @default.
• W2022081062 cites W2040381492 @default.
• W2022081062 cites W2042758661 @default.
• W2022081062 cites W2043676058 @default.
• W2022081062 cites W2044565924 @default.
• W2022081062 cites W2047630927 @default.
• W2022081062 cites W2057236986 @default.
• W2022081062 cites W2063857833 @default.
• W2022081062 cites W2064271701 @default.
• W2022081062 cites W2071367375 @default.
• W2022081062 cites W2072251446 @default.
• W2022081062 cites W2075801620 @default.
• W2022081062 cites W2080705428 @default.
• W2022081062 cites W2081494783 @default.
• W2022081062 cites W2083801916 @default.
• W2022081062 cites W2086654822 @default.
• W2022081062 cites W2087352977 @default.
• W2022081062 cites W2087919337 @default.
• W2022081062 cites W2095778701 @default.
• W2022081062 cites W2097114539 @default.
• W2022081062 cites W2099701147 @default.
• W2022081062 cites W2100774711 @default.
• W2022081062 cites W2101058683 @default.
• W2022081062 cites W2101998403 @default.
• W2022081062 cites W2104876262 @default.
• W2022081062 cites W2106828221 @default.
• W2022081062 cites W2106909888 @default.
• W2022081062 cites W2107187695 @default.
• W2022081062 cites W2107657759 @default.
• W2022081062 cites W2109598601 @default.
• W2022081062 cites W2111931048 @default.
• W2022081062 cites W2112742892 @default.
• W2022081062 cites W2112928630 @default.
• W2022081062 cites W2114312244 @default.
• W2022081062 cites W2114544212 @default.
• W2022081062 cites W2116811308 @default.
• W2022081062 cites W2118019823 @default.
• W2022081062 cites W2118487684 @default.
• W2022081062 cites W2119854546 @default.
• W2022081062 cites W2119871519 @default.
• W2022081062 cites W2121711582 @default.
• W2022081062 cites W2121887205 @default.
• W2022081062 cites W2123019342 @default.
• W2022081062 cites W2124418643 @default.
• W2022081062 cites W2125938458 @default.
• W2022081062 cites W2127242397 @default.
• W2022081062 cites W2127759081 @default.
• W2022081062 cites W2132886964 @default.
• W2022081062 cites W2135808445 @default.
• W2022081062 cites W2136051982 @default.
• W2022081062 cites W2138592928 @default.
• W2022081062 cites W2140253528 @default.
• W2022081062 cites W2140270616 @default.
• W2022081062 cites W2142400919 @default.
• W2022081062 cites W2142453430 @default.
• W2022081062 cites W2143859712 @default.
• W2022081062 cites W2146751158 @default.
• W2022081062 cites W2147951636 @default.
• W2022081062 cites W2147974324 @default.
• W2022081062 cites W2148937132 @default.
• W2022081062 cites W2149912063 @default.
• W2022081062 cites W2149993527 @default.

• next