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Polyamines are small amines that accumulate during stress and contribute to disease resistance through as yet unknown signaling pathways. Using a comprehensive RNA-sequencing analysis, we show that early transcriptional responses triggered by each of the most abundant polyamines (putrescine, spermidine, spermine, thermospermine and cadaverine) exhibit specific quantitative differences, suggesting that polyamines (rather than downstream metabolites) elicit defense responses. Signaling by putrescine, which accumulates in response to bacteria that trigger effector triggered immunity (ETI) and systemic acquired resistance (SAR), is largely dependent on the accumulation of hydrogen peroxide, and is partly dependent on salicylic acid (SA), the expression of ENHANCED DISEASE SUSCEPTIBILITY (EDS1) and NONEXPRESSOR of PR GENES1 (NPR1). Putrescine elicits local SA accumulation as well as local and systemic transcriptional reprogramming that overlaps with SAR. Loss-of-function mutations in arginine decarboxylase 2 (ADC2), which is required for putrescine synthesis and copper amine oxidase (CuAO), which is involved in putrescine oxidation, compromise basal defenses, as well as putrescine and pathogen-triggered systemic resistance. These findings confirm that putrescine elicits ROS-dependent SA pathways in the activation of plant defenses., (© 2020 John Wiley & Sons Ltd.)

We investigated the relationships of the two immune-regulatory plant metabolites, salicylic acid (SA) and pipecolic acid (Pip), in the establishment of plant systemic acquired resistance (SAR), SAR-associated defense priming, and basal immunity. Using SA-deficient sid2, Pip-deficient ald1, and sid2 ald1 plants deficient in both SA and Pip, we show that SA and Pip act both independently from each other and synergistically in Arabidopsis thaliana basal immunity to Pseudomonas syringae. Transcriptome analyses reveal that SAR establishment in Arabidopsis is characterized by a strong transcriptional response systemically induced in the foliage that prepares plants for future pathogen attack by preactivating multiple stages of defense signaling and that SA accumulation upon SAR activation leads to the downregulation of photosynthesis and attenuated jasmonate responses systemically within the plant. Whereas systemic Pip elevations are indispensable for SAR and necessary for virtually the whole transcriptional SAR response, a moderate but significant SA-independent component of SAR activation and SAR gene expression is revealed. During SAR, Pip orchestrates SA-dependent and SA-independent priming of pathogen responses in a FLAVIN-DEPENDENT-MONOOXYGENASE1 (FMO1)-dependent manner. We conclude that a Pip/FMO1 signaling module acts as an indispensable switch for the activation of SAR and associated defense priming events and that SA amplifies Pip-triggered responses to different degrees in the distal tissue of SAR-activated plants., (© 2016 American Society of Plant Biologists. All rights reserved.)

Cytokinins are phytohormones that are involved in various regulatory processes throughout plant development, but they are also produced by pathogens and known to modulate plant immunity. A novel transgenic approach enabling autoregulated cytokinin synthesis in response to pathogen infection showed that cytokinins mediate enhanced resistance against the virulent hemibiotrophic pathogen Pseudomonas syringae pv tabaci. This was confirmed by two additional independent transgenic approaches to increase endogenous cytokinin production and by exogenous supply of adenine- and phenylurea-derived cytokinins. The cytokinin-mediated resistance strongly correlated with an increased level of bactericidal activities and up-regulated synthesis of the two major antimicrobial phytoalexins in tobacco (Nicotiana tabacum), scopoletin and capsidiol. The key role of these phytoalexins in the underlying mechanism was functionally proven by the finding that scopoletin and capsidiol substitute in planta for the cytokinin signal: phytoalexin pretreatment increased resistance against P. syringae. In contrast to a cytokinin defense mechanism in Arabidopsis (Arabidopsis thaliana) based on salicylic acid-dependent transcriptional control, the cytokinin-mediated resistance in tobacco is essentially independent from salicylic acid and differs in pathogen specificity. It is also independent of jasmonate levels, reactive oxygen species, and high sugar resistance. The novel function of cytokinins in the primary defense response of solanaceous plant species is rather mediated through a high phytoalexin-pathogen ratio in the early phase of infection, which efficiently restricts pathogen growth. The implications of this mechanism for the coevolution of host plants and cytokinin-producing pathogens and the practical application in agriculture are discussed.

In incompatible plant-pathogen interactions, disease resistance is generated by rapid activation of a multitude of plant defence reactions. Little is known about the dependency of these resistance responses on external factors. The plasticity of plant defence mechanisms in terms of light conditions is studied here. Interaction of Arabidopsis thaliana (L.) Heynh. with an avirulent strain of Pseudomonas syringae pv. maculicola in the dark resulted in increased apoplastic bacterial growth and therefore reduced local resistance as compared to an infection process in the presence of light. Several characteristic defence reactions, including activation of phenylalanine ammonia-lyase, accumulation of salicylic acid (SA), expression of the pathogenesis-related protein PR-1 and the development of a microscopically defined hypersensitive response, proved to be light dependent. In contrast, the extent of the oxidative burst, as estimated by induction of the protectant gene glutathione- S-transferase, was not weakened by the absence of light. Moreover, pathogen-induced accumulation of jasmonic acid, production of the phytoalexin camalexin and transcriptional induction of a pathogen-inducible myrosinase were even more pronounced in the dark. Apart from affecting local defence responses, light also influenced the establishment of systemic acquired resistance (SAR). SAR development in response to infection by avirulent bacteria was completely lost when the primary infection process occurred in the absence of light. SAR developed both under medium (70 micromol photons m(-2) s(-1)) and strong (500 micromol photons m(-2) s(-1)) light conditions but was in the latter case not associated with an accumulation of SA and PR-1 in systemic leaves, demonstrating that SAR can be executed independently from these molecular SAR markers. Our results are consistent with the notion that SA accumulation in infected primary leaves is necessary for induction of systemic resistance and indicate that defence mechanisms different from SA signalling and PR-protein action exist in systemic tissue to confer resistance during SAR.

The bacterial elicitor flagellin induces a battery of immune responses in plants. However, the rates and intensities by which metabolically-related defenses develop upon flagellin-sensing are comparatively moderate. We report here that the systemic acquired resistance (SAR) inducer N-hydroxypipecolic acid (NHP) primes Arabidopsis thaliana plants for strongly enhanced metabolic and transcriptional responses to treatment by flg22, an elicitor-active peptide fragment of flagellin. While NHP powerfully activated priming of the flg22- induced accumulation of the phytoalexin camalexin, biosynthesis of the stress hormone salicylic acid (SA), generation of the NHP biosynthetic precursor pipecolic acid (Pip), and accumulation of the stress-inducible lipids γ-tocopherol and stigmasterol, it more modestly primed for the flg22-triggered generation of aromatic and branched-chain amino acids, and expression of FLG22-INDUCED RECEPTOR-KINASE1. The characterization of the biochemical and immune phenotypes of a set of different Arabidopsis single and double mutants impaired in NHP and/or SA biosynthesis indicates that, during earlier phases of the basal immune response of naïve plants to Pseudomonas syringae infection, NHP and SA mutually promote their biosynthesis and additively enhance camalexin formation, while SA prevents extraordinarily high NHP levels in later interaction periods. Moreover, SA and NHP additively contribute to Arabidopsis basal immunity to bacterial and oomycete infection, as well as to the flagellin-induced acquired resistance response that is locally observed in plant tissue exposed to exogenous flg22. Our data reveal mechanistic similarities and differences between the activation modes of flagellin-triggered acquired resistance in local tissue and the SAR state that is systemically induced in plants upon pathogen attack. They also corroborate that the NHP precursor Pip has no independent immune-related activity. [ABSTRACT FROM AUTHOR]

N‐hydroxypipecolic acid (NHP) accumulates in pathogen‐inoculated and distant leaves of the Arabidopsis shoot and induces systemic acquired resistance (SAR) in dependence of the salicylic acid (SA) receptor NPR1. We report here that SAR triggered by exogenous NHP treatment requires the function of the transcription factors TGA2/5/6 in addition to NPR1, and is further positively affected by TGA1/4. Consistently, a tga2/5/6 triple knockout mutant is fully impaired in NHP‐induced SAR gene expression, while a tga1/4 double mutant shows an attenuated, partial transcriptional response to NHP. Moreover, tga2/5/6 and tga1/4 exhibited fully and strongly impaired pathogen‐triggered SAR, respectively, while SA‐induced resistance was more moderately compromised in both lines. At the same time, tga2/5/6 was not and tga1/4 only partially impaired in the accumulation of NHP and SA at sites of bacterial attack. Strikingly, SAR gene expression in the systemic tissue induced by local bacterial inoculation or locally applied NHP fully required functional TGA2/5/6 and largely depended on TGA1/4 factors. The systemic accumulation of NHP and SA was attenuated but not abolished in the SAR‐compromised and transcriptionally blocked tga mutants, suggesting their transport from inoculated to systemic tissue. Our results indicate the existence of a critical TGA‐ and NPR1‐dependent transcriptional module that mediates the induction of SAR and systemic defence gene expression by NHP. Summary statement: N‐hydroxypipecolic acid activates plant systemic acquired resistance (SAR) and SAR gene expression via the transcription factors TGA2/5/6 and the coregulator NPR1. SAR is also promoted by TGA1/4, which mediates expression of a subset of SAR genes and supports the biosynthesis of SAR‐inducing hormones. [ABSTRACT FROM AUTHOR]

Summary: Expression of OXIDATIVE SIGNAL‐INDUCIBLE1 (OXI1) is induced by a number of stress conditions and regulates the interaction of plants with pathogenic and beneficial microbes.In this work, we generated Arabidopsis OXI1 knockout and genomic OXI1 overexpression lines and show by transcriptome, proteome, and metabolome analysis that OXI1 triggers ALD1, SARD4, and FMO1 expressions to promote the biosynthesis of pipecolic acid (Pip) and N‐hydroxypipecolic acid (NHP).OXI1 contributes to enhanced immunity by induced SA biosynthesis via CBP60g‐induced expression of SID2 and camalexin accumulation via WRKY33‐targeted transcription of PAD3. OXI1 regulates genes involved in reactive oxygen species (ROS) generation such as RbohD and RbohF. OXI1 knock out plants show enhanced expression of nuclear and chloroplast genes of photosynthesis and enhanced growth under ambient conditions, while OXI1 overexpressing plants accumulate NHP, SA, camalexin, and ROS and show a gain‐of‐function (GOF) cell death phenotype and enhanced pathogen resistance. The OXI1 GOF phenotypes are completely suppressed when compromising N‐hydroxypipecolic acid (NHP) synthesis in the fmo1 or ald1 background, showing that OXI1 regulation of immunity is mediated via the NHP pathway.Overall, these results show that OXI1 plays a key role in basal and effector‐triggered plant immunity by regulating defense and programmed cell death via biosynthesis of salicylic acid, N‐hydroxypipecolic acid, and camalexin. [ABSTRACT FROM AUTHOR]

Recent work has provided evidence for the occurrence of N -hydroxypipecolic acid (NHP) in Arabidopsis thaliana , characterized its pathogen-inducible biosynthesis by a three-step metabolic sequence from l -lysine, and established a central role for NHP in the regulation of systemic acquired resistance. Here, we show that NHP is biosynthesized in several other plant species in response to microbial attack, generally together with its direct metabolic precursor pipecolic acid and the phenolic immune signal salicylic acid. For example, NHP accumulates locally in inoculated leaves and systemically in distant leaves of cucumber in response to Pseudomonas syringae attack, in Pseudomonas -challenged tobacco and soybean leaves, in tomato inoculated with the oomycete Phytophthora infestans , in leaves of the monocot Brachypodium distachyon infected with bacterial (Xanthomonas translucens) and fungal (Magnaporthe oryzae) pathogens, and in M. oryzae -inoculated barley. Notably, resistance assays indicate that NHP acts as a potent inducer of acquired resistance to bacterial and fungal infection in distinct monocotyledonous and dicotyledonous species. Pronounced systemic accumulation of NHP in leaf phloem sap of locally inoculated cucumber supports a function for NHP as a phloem-mobile immune signal. Our study thus generalizes the existence and function of an NHP resistance pathway in plant systemic acquired resistance. [ABSTRACT FROM AUTHOR]

Recent research has established that the pipecolate pathway, a three-step biochemical sequence from l -lysine to N -hydroxypipecolic acid (NHP), is central for plant systemic acquired resistance (SAR). NHP orchestrates SAR establishment in concert with the immune signal salicylic acid (SA). Here, we outline the biochemistry of NHP formation from l -Lys and address novel progress on SA biosynthesis in Arabidopsis and other plant species. In Arabidopsis, the pathogen-inducible pipecolate and salicylate pathways are activated by common and distinct regulatory elements and mutual interactions between both metabolic branches exist. The mode of action of NHP in SAR involves direct induction of SAR gene expression, signal amplification, priming for enhanced defense activation and positive interplay with SA signaling to ensure elevated plant immunity. [ABSTRACT FROM AUTHOR]

Summary: Members of the MILDEW RESISTANCE LOCUS O (MLO) gene family confer susceptibility to powdery mildews in different plant species, and their existence therefore seems to be disadvantageous for the plant. We recognized that expression of the Arabidopsis MLO2 gene is induced after inoculation with the bacterial pathogen Pseudomonas syringae, promoted by salicylic acid (SA) signaling, and systemically enhanced in the foliage of plants exhibiting systemic acquired resistance (SAR). Importantly, distinct mlo2 mutant lines were unable to systemically increase resistance to bacterial infection after inoculation with P. syringae, indicating that the function of MLO2 is necessary for biologically induced SAR in Arabidopsis. Our data also suggest that the close homolog MLO6 has a supportive but less critical role in SAR. In contrast to SAR, basal resistance to bacterial infection was not affected in mlo2. Remarkably, SAR‐defective mlo2 mutants were still competent in systemically increasing the levels of the SAR‐activating metabolites pipecolic acid (Pip) and SA after inoculation, and to enhance SAR‐related gene expression in distal plant parts. Furthermore, although MLO2 was not required for SA‐ or Pip‐inducible defense gene expression, it was essential for the proper induction of disease resistance by both SAR signals. We conclude that MLO2 acts as a critical downstream component in the execution of SAR to bacterial infection, being required for the translation of elevated defense responses into disease resistance. Moreover, our data suggest a function for MLO2 in the activation of plant defense priming during challenge by P. syringae. [ABSTRACT FROM AUTHOR]

Genome-wide microarray analyses revealed that during biological activation of systemic acquired resistance (SAR) in Arabidopsis, the transcript levels of several hundred plant genes were consistently up- (SAR+ genes) or down-regulated (SAR- genes) in systemic, non-inoculated leaf tissue. This transcriptional reprogramming fully depended on the SAR regulator FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1). Functional gene categorization showed that genes associated with salicylic acid (SA)-associated defenses, signal transduction, transport, and the secretory machinery are overrepresented in the group of SAR+ genes, and that the group of SAR- genes is enriched in genes activated via the jasmonate (JA)/ethylene (ET)-defense pathway, as well as in genes associated with cell wall remodeling and biosynthesis of constitutively produced secondary metabolites. This suggests that SAR-induced plants reallocate part of their physiological activity from vegetative growth towards SA-related defense activation. Alignment of the SAR expression data with other microarray information allowed us to define three clusters of SAR+ genes. Cluster I consists of genes tightly regulated by SA. Cluster II genes can be expressed independently of SA, and this group is moderately enriched in H2O2- and abscisic acid (ABA)-responsive genes. The expression of the cluster III SAR+ genes is partly SA-dependent. We propose that SA-independent signaling events in early stages of SAR activation enable the biosynthesis of SA and thus initiate SA-dependent SAR signaling. Both SA-independent and SA-dependent events tightly co-operate to realize SAR. SAR+ genes function in the establishment of diverse resistance layers, in the direct execution of resistance against different (hemi-)biotrophic pathogen types, in suppression of the JA- and ABA-signaling pathways, in redox homeostasis, and in the containment of defense response activation. Our data further indicated that SAR-associated defense priming can be realized by partial pre-activation of particular defense pathways. [ABSTRACT FROM AUTHOR]

Metabolic signals orchestrate plant defenses against microbial pathogen invasion. Here, we report the identification of the non-protein amino acid pipecolic acid (Pip), a common Lys catabolite in plants and animals, as a critical regulator of inducible plant immunity. Following pathogen recognition, Pip accumulates in inoculated Arabidopsis thaliana leaves, in leaves distal from the site of inoculation, and, most specifically, in petiole exudates from inoculated leaves. Defects of mutants in AGD2-LIKE DEFENSE RESPONSE PROTEIN1 (ALD1) in systemic acquired resistance (SAR) and in basal, specific, and β-aminobutyric acid–induced resistance to bacterial infection are associated with a lack of Pip production. Exogenous Pip complements these resistance defects and increases pathogen resistance of wild-type plants. We conclude that Pip accumulation is critical for SAR and local resistance to bacterial pathogens. Our data indicate that biologically induced SAR conditions plants to more effectively synthesize the phytoalexin camalexin, Pip , and salicylic acid and primes plants for early defense gene expression. Biological priming is absent in the pipecolate-deficient ald1 mutants. Exogenous pipecolate induces SAR -related defense priming and partly restores priming responses in ald1. We conclude that Pip orchestrates defense amplification, positive regulation of salicylic acid biosynthesis, and priming to guarantee effective local resistance induction and the establishment of SAR. [ABSTRACT FROM AUTHOR]

Upon inoculation with pathogenic microbes, plants induce an array of metabolic changes that potentially contribute to induced resistance or even enhance susceptibility. When analysing leaf lipid composition during the Arabidopsis thaliana–Pseudomonas syringae interaction, we found that accumulation of the phytosterol stigmasterol is a significant plant metabolic process that occurs upon bacterial leaf infection. Stigmasterol is synthesized from β-sitosterol by the cytochrome P450 CYP710A1 via C22 desaturation . Arabidopsis cyp710A1 mutant lines impaired in pathogen-inducible expression of the C22 desaturase and concomitant stigmasterol accumulation are more resistant to both avirulent and virulent P. syringae strains than wild-type plants, and exogenous application of stigmasterol attenuates this resistance phenotype. These data indicate that induced sterol desaturation in wild-type plants favours pathogen multiplication and plant susceptibility. Stigmasterol formation is triggered through perception of pathogen-associated molecular patterns such as flagellin and lipopolysaccharides, and through production of reactive oxygen species, but does not depend on the salicylic acid, jasmonic acid or ethylene defence pathways. Isolated microsomal and plasma membrane preparations exhibited a similar increase in the stigmasterol/β-sitosterol ratio as whole-leaf extracts after leaf inoculation with P. syringae, indicating that the stigmasterol produced is incorporated into plant membranes. The increased contents of stigmasterol in leaves after pathogen attack do not influence salicylic acid-mediated defence signalling but attenuate pathogen-induced expression of the defence regulator flavin-dependent monooxygenase 1. P. syringae thus promotes plant disease susceptibility through stimulation of sterol C22 desaturation in leaves, which increases the stigmasterol to β-sitosterol ratio in plant membranes. [ABSTRACT FROM AUTHOR]

Systemic acquired resistance (SAR) develops in response to local microbial leaf inoculation and renders the whole plant more resistant to subsequent pathogen infection. Accumulation of salicylic acid (SA) in noninfected plant parts is required for SAR, and methyl salicylate (MESA) and jasmonate (JA) are proposed to have critical roles during SAR long-distance signaling from inoculated to distant leaves. Here, we address the significance of MeSA and JA during SAR development in Arabidopsis thaliana. MeSA production increases in leaves inoculated with the SAR-inducing bacterial pathogen Pseudomonas syringae; however, most MeSA is emitted into the atmosphere, and only small amounts are retained. We show that in several Arabidopsis defense mutants, the abilities to produce MeSA and to establish SAR do not coincide. T-DNA insertion lines defective in expression of a pathogen-responsive SA methyltransferase gene are completely devoid of induced MeSA production but increase systemic SA levels and develop SAR upon local P. syringae inoculation. Therefore, MeSA is dispensable for SAR in Arabidopsis, and SA accumulation in distant leaves appears to occur by de novo synthesis via isochorismate synthase. We show that MeSA production induced by P. syringae depends on the JA pathway but that JA biosynthesis or downstream signaling is not required for SAR. In compatible interactions, MeSA production depends on the P. syringae virulence factor coronatine, suggesting that the phytopathogen uses coronatine-mediated volatilization of MeSA from leaves to attenuate the SA-based defense pathway. [ABSTRACT FROM AUTHOR]

Although interactions of plants with virulent and avirulent host pathogens are under intensive study, relatively little is known about plant interactions with non-adapted pathogens and the molecular events underlying non-host resistance. Here we show that two Pseudomonas syringae strains for which Arabidopsis is a non-host plant, P. syringae pathovar (pv.) glycinea (Psg) and P. syringae pv. phaseolicola (Psp),induce salicylic acid (SA) accumulation and pathogenesis-related gene expression at inoculation sites, and that induction of these defences is largely dependent on bacterial type III secretion. The defence signalling components activated by non-adapted bacteria resemble those initiated by host pathogens, including SA, non-expressor of PR-1, non-race specific disease resistance 1, phytoalexin-deficient 4 and enhanced disease susceptibility 1. However, some differences in individual defence pathways induced by Psg and Psp exist, suggesting that for each strain, distinct sets of type III effectors are recognized by the plant. Although induction of SA-related defences occurs, it does not directly contribute to bacterial non-host resistance, because Arabidopsis mutants compromised in SA signalling and other classical defence pathways do not permit enhanced survival of Psg or Psp in leaves. The finding that numbers of non-adapted bacteria in leaf extracellular spaces rapidly decline after inoculation suggests that they fail to overcome toxic or structural defence barriers preceding SA-related responses. Consistent with this hypothesis, rapid, type III secretion system-independent upregulation of the lignin biosynthesis genes, PAL1 and BCB, which might contribute to an early induced, cell wall-based defence mechanism, occurs in response to non-adapted bacteria. Moreover, knockout of PAL1 permits increased leaf survival of non-host bacteria. In addition, different survival rates of non-adapted bacteria in leaves from Arabidopsis accessions and mutants with distinct glucosinolate composition or hydrolysis exist. Possible roles for early inducible, cell wall-based defences and the glucosinolate/myrosinase system in bacterial non-host resistance are discussed. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) has been proposed to act as a factor delaying leaf senescence and fruit maturation in plants. Here we show that expression of a NO degrading dioxygenase (NOD) in Arabidopsis thaliana initiates a senescence-like phenotype, an effect that proved to be more pronounced in older than in younger leaves. This senescence phenotype was preceded by a massive switch in gene expression in which photosynthetic genes were down-regulated, whereas many senescence-associated genes (SAGs) and the 1-aminocyclopropane-1-carboxylic acid (ACC) synthase gene ACS6 involved in ethylene synthesis were up-regulated. External fumigation of NOD plants with NO as well as environmental conditions known to stimulate endogenous NO production attenuated the induced senescence programme. For instance, both high light conditions and nitrate feeding reduced the senescence phenotype and attenuated the down-regulation of photosynthetic genes as well as the up-regulation of SAGs. Treatment of plants with the cytokinin 6-benzylaminopurin (BAP) reduced the down-regulation of photosynthesis, although it had no consistent effect on SAG expression. Metabolic changes during NOD-induced senescence comprehended increases in salicylic acid (SA) levels, accumulation of the phytoalexin camalexin and elevation of leaf γ-tocopherol contents, all of which occurred during natural senescence in Arabidopsis leaves as well. Moreover, NO fumigation delayed the senescence process induced by darkening individual Arabidopsis Columbia-0 (Col-0) leaves. Our data thus support the notion that NO acts as a negative regulator of leaf senescence. [ABSTRACT FROM AUTHOR]

Abstract: Despite the identification of several key mechanisms underlying disease resistance, comparatively little is known about the way developmental factors affect the capability of plants to defend themselves against microbial pathogens. Here, the influence of leaf age on inducible local and systemic defence responses in the incompatible interaction between Arabidopsis thaliana and Pseudomonas syringae pv. maculicola (avrRPM1) is investigated. Comparison of the local defence behaviour of rosette leaves differing in age revealed that younger leaves generally had to invest in more pronounced inducible defences than older (non-senescent) leaves to achieve a similar degree of resistance. For instance, younger leaves exhibited a more distinctive oxidative burst and a stronger hypersensitive cell death response than older ones. The pathogen-induced expression of the defence related genes phenylalanine ammonia lyase (PAL) and glutathione-S-transferase (GST) proved to be higher and faster in younger leaves, respectively, whereas gene induction of PR-1 (pathogenesis-related protein 1) was largely independent of leaf age. Similarly, upon bacterial inoculation, the defence signal salicylic acid (SA) and the phytoalexin camalexin accumulated to higher amounts in younger than in older leaves. Despite these differences in inducible defences, bacterial growth as a measure of disease resistance proved to be similar in inoculated younger and older leaves. In tissue distant from the inoculation site, systemic acquired resistance (SAR) developed most effectively in younger leaves, and this response was associated with strong accumulation of SA and PR-1 transcripts. However, older leaves still exhibited SAR to a certain degree, and this resistance developed essentially without systemic SA or PR-1 accumulation. These results suggest that mechanisms independent of SA signalling in systemic leaves contribute to realise SAR. [Copyright &y& Elsevier]

Plants achieve an optimal balance between growth and defense by a fine-tuned biosynthesis and metabolic inactivation of immune-stimulating small molecules. Recent research illustrates that three common hubs are involved in the cooperative regulation of systemic acquired resistance (SAR) by the defense hormones N-hydroxypipecolic acid (NHP) and salicylic acid (SA). First, a common set of regulatory proteins is involved in their biosynthesis. Second, NHP and SA are glucosylated by the same glycosyltransferase, UGT76B1, and thereby inactivated in concert. And third, NHP confers immunity via the SA receptor NPR1 to reprogram plants at the level of transcription and primes plants for an enhanced defense capacity. An overview of SA and NHP metabolism is provided, and their contribution to long-distance signaling in SAR is discussed. [ABSTRACT FROM AUTHOR]