Induction of systemic resistance in tomato by <i>N</i>‐acyl‐L‐homoserine lactone‐producing rhizosphere bacteria

Schuhegger, Regina; Ihring, Alexandra; Gantner, Stephan; Bahnweg, G.; Knappe, Claudia; Vogg, Gerd; Hutzler, Peter; Schmid, Michael; Breusegem, Frank Van; Eberl, Leo; Hartmann, Anton; Langebartels, Christian

doi:10.1111/j.1365-3040.2005.01471.x

Cited by 416 publications

(297 citation statements)

References 48 publications

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“…The pathogenesis-related gene P4 in tomato (GenBank gene identifier 544185) is homologous to PR1a in tobacco (Nicotiana tabacum) and Arabidopsis and is up-regulated in response to exogenous SA and its analog benzothiadiazole (Van Kan et al, 1995;Fidantsef et al, 1999;Schuhegger et al, 2006) as well as in response to the ethylene mimic ethephon (Van Kan et al, 1995;Chao et al, 1999). The proteinase inhibitor gene PI-II (GenBank gene identifier 543955) is transcriptionally activated in response to JAs and also ethylene (Farmer et al, 1992;Ohtsubo et al, 1999).…”

Section: Loss Of Function Of Fad7 Enhances P4 Expression and Local Samentioning

confidence: 99%

Loss of Function of FATTY ACID DESATURASE7 in Tomato Enhances Basal Aphid Resistance in a Salicylate-Dependent Manner

et al. 2012

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We report here that disruption of function of the v-3 FATTY ACID DESATURASE7 (FAD7) enhances plant defenses against aphids. The suppressor of prosystemin-mediated responses2 (spr2) mutation in tomato (Solanum lycopersicum), which eliminates the function of FAD7, reduces the settling behavior, survival, and fecundity of the potato aphid (Macrosiphum euphorbiae). Likewise, the antisense suppression of LeFAD7 expression in wild-type tomato plants reduces aphid infestations. Aphid resistance in the spr2 mutant is associated with enhanced levels of salicylic acid (SA) and mRNA encoding the pathogenesis-related protein P4. Introduction of the Naphthalene/salicylate hydroxylase transgene, which suppresses SA accumulation, restores wild-type levels of aphid susceptibility to spr2. Resistance in spr2 is also lost when we utilize virus-induced gene silencing to suppress the expression of NONEXPRESSOR OF PATHOGENESIS-RELATED PROTEINS1 (NPR1), a positive regulator of many SAdependent defenses. These results indicate that FAD7 suppresses defenses against aphids that are mediated through SA and NPR1. Although loss of function of FAD7 also inhibits the synthesis of jasmonate (JA), the effects of this desaturase on aphid resistance are not dependent on JA; other mutants impaired in JA synthesis (acx1) or perception (jai1-1) show wild-type levels of aphid susceptibility, and spr2 retains aphid resistance when treated with methyl jasmonate. Thus, FAD7 may influence JAdependent defenses against chewing insects and SA-dependent defenses against aphids through independent effects on JA synthesis and SA signaling. The Arabidopsis (Arabidopsis thaliana) mutants Atfad7-2 and Atfad7-1fad8 also show enhanced resistance to the green peach aphid (Myzus persicae) compared with wild-type controls, indicating that FAD7 influences plantaphid interactions in at least two plant families.

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Section: Loss Of Function Of Fad7 Enhances P4 Expression and Local Samentioning

confidence: 99%

Loss of Function of FATTY ACID DESATURASE7 in Tomato Enhances Basal Aphid Resistance in a Salicylate-Dependent Manner

et al. 2012

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“…The siderophore pyochelin and the antibiotic pyocyanin are both required for the induction of systemic resistance in tomato by P. aeruginosa 7NSK2 (Audenaert et al 2002). QS N-acylhomoserine lactones were recently shown to act as inducers of systemic resistance in tomato against Alternaria alternata (Shuhegger et al 2006). The compound 2,3-butanediol is produced by Bacillus spp.…”

Section: Induction Of Systemically Induced Resistance In the Plantmentioning

confidence: 99%

“…Analysis of the reaction of tomato to the ISR-eliciting strain Serratia liquefaciens MG1, using a macroarray containing cDNA probes of 70 defence-related and signalling genes, revealed enhanced expression of 12 genes. Seven of those coded for PRs, whereas the others were involved in oxidative stress, ethylene signalling, or metabolism (Shuhegger et al 2006).…”

Section: Expression Of Systemically Induced Resistance In the Plantmentioning

confidence: 99%

Plant responses to plant growth-promoting rhizobacteria

2007

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Non-pathogenic soilborne microorganisms can promote plant growth, as well as suppress diseases. Plant growth promotion is taken to result from improved nutrient acquisition or hormonal stimulation. Disease suppression can occur through microbial antagonism or induction of resistance in the plant. Several rhizobacterial strains have been shown to act as plant growth-promoting bacteria through both stimulation of growth and induced systemic resistance (ISR), but it is not clear in how far both mechanisms are connected. Induced resistance is manifested as a reduction of the number of diseased plants or in disease severity upon subsequent infection by a pathogen. Such reduced disease susceptibility can be local or systemic, result from developmental or environmental factors and depend on multiple mechanisms. The spectrum of diseases to which PGPRelicited ISR confers enhanced resistance overlaps partly with that of pathogen-induced systemic acquired resistance (SAR). Both ISR and SAR represent a state of enhanced basal resistance of the plant that depends on the signalling compounds jasmonic acid and salicylic acid, respectively, and pathogens are differentially sensitive to the resistances activated by each of these signalling pathways. Root-colonizing Pseudomonas bacteria have been shown to alter plant gene expression in roots and leaves to different extents, indicative of recognition of one or more bacterial determinants by specific plant receptors. Conversely, plants can alter root exudation and secrete compounds that interfere with quorum sensing (QS) regulation in the bacteria. Such two-way signalling resembles the interaction of root-nodulating Rhizobia with legumes and between mycorrhizal fungi and roots of the majority of plant species. Although ISR-eliciting rhizobacteria can induce typical early defence-related responses in cell suspensions, in plants they do not necessarily activate defence-related gene expression. Instead, they appear to act through priming of effective resistance mechanisms, as reflected by earlier and stronger defence reactions once infection occurs.

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“…Accumulated evidence demonstrates that both nitric oxide (NO) and hydrogen peroxide (H 2 O 2 ) are signals to participate in multiple physiological processes, including systemic acquired resistance, the hypersensitive response, leaf senescence, programmed cell death, stomatal closure, root gravitropism, cell wall development, pollen-stigma interaction, and development (Grant and Loake, 2000;Neill et al, 2002;Pagnussat et al, 2003;Hu et al, 2004;Mittler et al, 2004;Schuhegger et al, 2006;Xuan et al, 2008). Adventitious roots are derived primarily from plant stems and are essential for plant adaptation to environmental stress; studying the adventitious root formation is also significant for both fundamental and applied plant biology.…”

mentioning

confidence: 99%

N-3-Oxo-Decanoyl-l-Homoserine-Lactone Activates Auxin-Induced Adventitious Root Formation via Hydrogen Peroxide- and Nitric Oxide-Dependent Cyclic GMP Signaling in Mung Bean

et al. 2011

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N-Acyl-homoserine-lactones (AHLs) are bacterial quorum-sensing signaling molecules that regulate population density. Recent evidence demonstrates their roles in plant defense responses and root development. Hydrogen peroxide (H 2 O 2 ), nitric oxide (NO), and cyclic GMP (cGMP) are essential messengers that participate in various plant physiological processes, but how these messengers modulate the plant response to N-acyl-homoserine-lactone signals remains poorly understood. Here, we show that the N-3-oxo-decanoyl-homoserine-lactone (3-O-C10-HL), in contrast to its analog with an unsubstituted branch chain at the C3 position, efficiently stimulated the formation of adventitious roots and the expression of auxin-response genes in explants of mung bean (Vigna radiata) seedlings. This response was mimicked by the exogenous application of auxin, H 2 O 2 , NO, or cGMP homologs but suppressed by treatment with scavengers or inhibitors of H 2 O 2 , NO, or cGMP metabolism. The 3-O-C10-HL treatment enhanced auxin basipetal transport; this effect could be reversed by treatment with H 2 O 2 or NO scavengers but not by inhibitors of cGMP synthesis. Inhibiting 3-O-C10-HL-induced H 2 O 2 or NO accumulation impaired auxin-or 3-O-C10-HL-induced cGMP synthesis; however, blocking cGMP synthesis did not affect auxin-or 3-O-C10-HLinduced H 2 O 2 or NO generation. Additionally, cGMP partially rescued the inhibitory effect of H 2 O 2 or NO scavengers on 3-O-C10-HL-induced adventitious root development and auxin-response gene expression. These results suggest that 3-O-C10-HL, unlike its analog with an unmodified branch chain at the C3 position, can accelerate auxin-dependent adventitious root formation, possibly via H 2 O 2 -and NO-dependent cGMP signaling in mung bean seedlings.

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Induction of systemic resistance in tomato by N‐acyl‐L‐homoserine lactone‐producing rhizosphere bacteria

Cited by 416 publications

References 48 publications

Loss of Function of FATTY ACID DESATURASE7 in Tomato Enhances Basal Aphid Resistance in a Salicylate-Dependent Manner

Loss of Function of FATTY ACID DESATURASE7 in Tomato Enhances Basal Aphid Resistance in a Salicylate-Dependent Manner

Plant responses to plant growth-promoting rhizobacteria

N-3-Oxo-Decanoyl-l-Homoserine-Lactone Activates Auxin-Induced Adventitious Root Formation via Hydrogen Peroxide- and Nitric Oxide-Dependent Cyclic GMP Signaling in Mung Bean

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