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Prior to Ginkgo leaf harvest, we implemented four exogenous applications of salicylic acid (SA: 50, 80, and 100 mg * [L.sup.-1]) or methyl jasmonate (MJ: 20, 40, and 80 mg * [L.sup.-1]) as leaf spray to investigate their effect on flavonoids content and related enzyme activity. Compared with the control, a significant increase of 12% and 26% in flavonoid content was observed 7 days after the first application of 100 mg * [L.sup.-1] SA and 20 mg * [L.sup.-1] MJ, respectively; both were determined to be the best treatments. Operationally, administering either elicitor (SA or MJ) 1 week prior to leaf harvest is deemed to be the most practical and economic option. Additionally, enzymes activity involved in flavonoid metabolism (phenylalanine ammonialyase, cinnamate 4-hydroxylase, and 4-coumarate:coenzyme A ligase) and antioxidants (peroxidase, superoxide dismutase, and catalase) significantly increased in most SA and MJ treatments. The results strongly support Ginkgo leaf response to SA- or MJ-induced stress through increased nonenzymatic antioxidant compounds (flavonoids) and activity of antioxidant enzymes. Key words: Ginkgo leaves, flavonoids, antioxidant enzymes, salicylic acid, methyl jasmonate. Avant la recolte des feuilles de Ginkgo, nous avons procede a quatre vaporisations foliaires d'acide salicylique (AS : 50, 80 et 100 mg * [L.sup.-1]) ou de jasmonate de methyle (JM : 20, 40 et 80 mg * [L.sup.-1]) pour etudier leur effet sur la teneur en flavonoides et l'activite enzymatique associee. Comparativement au temoin, une augmentation significative de 12 et 26 % de la teneur en flavonoides a ete observee sept jours apres la premiere application de respectivement 100 mg * [L.sup.-1] de AS et 20 mg * [L.sup.-1] de JM; ces deux traitements etaient les meilleurs. De facon operationnelle, l'application de l'un ou l'autre des eliciteurs (AS ou JM) une semaine avant la recolte des feuilles est consideree comme l'option la plus pratique et la plus economique. De plus, l'activite des enzymes impliquees dans le metabolisme des flavonoides (phenylalanine ammonia-lyase, cinnamate 4-hydroxylase, et 4-coumarate : CoA ligase) et des antioxydants (peroxydase, superoxyde dismutase et catalase) ont significativement augmente dans la plupart des traitements avec AS et JM. Les resultats concordent etroitement avec la reaction des feuilles de Ginkgo au stress induit par AS et JM par le biais de l'augmentation de la teneur en composes antioxydants (flavonoides) et de l'activite des enzymes antioxydantes. [Traduit par la Redaction] Mots-cles : feuilles de Ginkgo, flavonoides, enzymes antioxydantes, acide salicylique, jasmonate de methyle., Introduction Ginkgo biloba L., commonly known as Ginkgo, is a native Chinese tree species whose leaves have been used in ancient traditional medicine. The medicinal applications of Ginkgo leaf extract [...]

A genetically tractable model plant pathosystem, Pseudomonas syringae pv. tomato DC3000 on tomato and Arabidopsis thaliana hosts, was used to investigate the role of salicylic acid (SA) and iron acquisition via siderophores in bacterial virulence. Pathogen-induced SA accumulation mediates defense in these plants, and DC3000 contains the genes required for the synthesis of SA, the SA-incorporated siderophore yersiniabactin (Ybt), and the fluorescent siderophore pyoverdin (Pvd). We found that DC3000 synthesizes SA, Ybt, and Pvd under iron-limiting conditions in culture. Synthesis of SA and Ybt by DC3000 requires pchA, an isochorismate synthase gene in the Ybt genomic cluster, and exogenous SA can restore Ybt production by the pchA mutant. Ybt was also produced by DC3000 in planta, suggesting that Ybt plays a role in DC3000 pathogenesis. However, the pchA mutant did not exhibit any growth defect or altered virulence in plants. This lack of phenotype was not attributable to plant-produced SA restoring Ybt production, as the pchA mutant grew similarly to DC3000 in an Arabidopsis SA biosynthetic mutant, and in planta Ybt was not detected in pchA-infected wild-type plants. In culture, no growth defect was observed for the pchA mutant versus DC3000 for any condition tested. Instead, enhanced growth of the pchA mutant was observed under stringent iron limitation and additional stresses. This suggests that SA and Ybt production by DC3000 is costly and that Pvd is sufficient for iron acquisition. Further exploration of the comparative synthesis and utility of Ybt versus Pvd production by DC3000 found siderophore-dependent amplification of ybt gene expression to be absent, suggesting that Ybt may play a yet unknown role in DC3000 pathogenesis.

Agrobacterium tumefaciens is capable of transferring and integrating an oncogenic T-DNA (transferred DNA) from its tumor-inducing (Ti) plasmid into dicotyledonous plants. This transfer requires that the virulence genes (vir regulon) be induced by plant signals such as acetosyringone in an acidic environment. Salicylic acid (SA) is a key signal molecule in regulating plant defense against pathogens. However, how SA influences Agrobacterium and its interactions with plants is poorly understood. Here we show that SA can directly shut down the expression of the vir regulon. SA specifically inhibited the expression of the Agrobacterium virA/G two-component regulatory system that tightly controls the expression of the vir regulon including the repABC operon on the Ti plasmid. We provide evidence suggesting that SA attenuates the function of the VirA kinase domain. Independent of its effect on the vir regulon, SA up-regulated the attKLM operon, which functions in degrading the bacterial quormone N-acylhomoserine lactone. Plants defective in SA accumulation were more susceptible to Agrobacterium infection, whereas plants overproducing SA were relatively recalcitrant to tumor formation. Our results illustrate that SA, besides its well known function in regulating plant defense, can also interfere directly with several aspects of the Agrobacterium infection process. two-component system | tumorigenesis | defense response | rhizosphere plant-microbe interaction

In plants, salicylic acid (SA) plays an important role in signaling both local and systemic defense responses. Previous efforts to identify SA effector proteins in tobacco have led to the isolation of two soluble cytoplasmic SA-binding proteins (SABPs): catalase, SABP, and an [approximately equal to] 25-kDa protein, SABP2. Here we describe the identification of an SA-binding protein, SABP3, in the stroma of tobacco chloroplasts. SABP3 bound SA with an apparent dissociation constant ([K.sub.d]) of 3.7 [micro]M and exhibited much greater affinity for biologically active than inactive analogs. Purification and partial sequencing of SABP3 indicated that it is the chloroplast carbonic anhydrase (CA). Confirming this finding, recombinant tobacco chloroplast CA exhibited both CA enzymatic and SA-binding activities. Expression of this protein in yeast also demonstrated that CA/SABP3 has antioxidant activity. A second gene encoding CA was also cloned, and its encoded protein was shown to behave similarly to that purified as SABP3. Finally, silencing of CA gene expression in leaves suppressed the Pto:avrPto-mediated hypersensitive response in disease resistance. These results demonstrate that SA may act through multiple effector proteins in plants and shed further light on the function of CA in chloroplasts.

Research has been conducted on the bismuth heterobimetallic complexes. The synthesis and characterization of these complexes have been carried out and the results indicate that the complexes are soluble in common organic solvents and have better stability against hydrolysis.

We investigated the transport of salicylic acid and L-lactic acid across the placenta using the human trophoblast cell line BeWo. We performed uptake experiments and measured the change in intracellular pH ([pH.sup.i]). The uptakes of [[sup.14]C] salicylic acid and L-[[sup.14]C]lactic acid were temperature- and extracellular pH-dependent and saturable at higher concentrations. Both uptakes were also reduced by FCCP, nigericin, and NA[N.sub.3]. Various nonsteroidal anti-inflammatory drugs (NSAIDs) strongly inhibited the uptake of L-[[sup.14]C]lactic acid. Salicylic acid and ibuprofen noncompetitively inhibited the uptake of L-[[sup.14]C]lactic acid. [alpha]-Cyano-4-hydroxycinnamate (CHC), a monocarboxylate transporter inhibitor, suppressed the uptake of L-[[sup.14]C]lactic acid but not that of [[sup.14]C]salicylic acid. CHC also suppressed the decrease of [pH.sub.i] induced by L-lactic acid but had little effect on that induced by salicylic acid or diclofenac. These results suggest that NSAIDs are potent inhibitors of lactate transporters, although they are transported mainly by a transport system distinct from that for L-lactic acid. L-lactic acid; blood-placental barrier; monocarboxylate transporter; [alpha]-cyano-4-hydroxycinnamate; intracellular pH

Salicylate is converted to 3- and 5-hydroxysalicylate or gentisate in the presence of oxygen in cell extracts of Pseudaminobacter salicylatoxidans strain BN12. Data show that gentisate is formed by direct ring fision of salicylate, catalyzed by a 1,2-dioxygenase reaction.

Results reveal that the pmsCEAB contains genes for salicylic acid genes and their expression is regulated by iron in Pseudomonas fluorescens WCS374. Data further indicate that salicylic acid and pseudomonine siderophore biosynthesis in WCS374 are related.

Results show that in the presence of biphenyl, the dibenzofuran is cometabolized in Ralstonia sp. SBUG 290 to give rise to hydroxylated dibenzofuran compound. Data indicate that the compound is degraded via salicyclic acid using a lateral dioxygenation pathway.

In recent years, it has become apparent that salicylic acid (SA) plays an important role in plant defense responses to pathogen attack. Previous studies have suggested that one of SA's mechanisms of action is the inhibition of catalase, resulting in elevated levels of [H.sub.2][O.sub.2], which activate defense-related genes. Here we demonstrate that SA also inhibits ascorbate peroxidase (APX), the other key enzyme for scavenging [H.sub.2][O.sub.2]. The synthetic inducer of defense responses, 2,6-dichloroisonicotinic acid (INA), was also found to be an effective inhibitor of APX. In the presence of 750 [mu]M ascorbic acid (AsA), substrate-dependent [IC.sub.50] values of 78 [mu]M and 95 [mu]M were obtained for SA and INA, respectively. Furthermore, the ability of SA analogues to block APX activity correlated with their ability to induce defense-related genes in tobacco and enhance resistance to tobacco mosaic virus. Inhibition of APX by SA appears to be reversible, thus differing from the time-dependent, irreversible inactivation by suicide substrates such as p-aminophenol. In contrast to APX, the guaiacol-utilizing peroxidases, which participate in the synthesis and crosslinking of cell wall components as part of the defense response, are not inhibited by SA or INA. The inhibition of both catalase and APX, but not guaiacol peroxidases, supports the hypothesis that SA-induced defense responses are mediated, in part, through elevated [H.sub.2][O.sub.2] levels or coupled perturbations of the cellular redox state.

2,6-Dichloroisonicotinic acid (INA) and salicylic acid (SA) are potent inducers of plant defense responses including the synthesis of pathogenesis-related (PR) proteins and the development of enhanced disease resistance. A soluble SA-binding protein has been purified from tobacco with an affinity and specificity of binding that suggest it is a SA receptor. Recently, this protein has been shown to be a catalase whose enzymatic activity is inhibited by SA binding. We have proposed that the resulting increase in intracellular levels of reactive oxygen species plays a role in the induction of defense responses such as PR protein gene expression. Here we report that INA, like SA, binds the SA-binding protein/catalase and inhibits its enzymatic activity. In fact, the dose-response curves for inhibition of catalase by these two compounds are similar. Furthermore, the ability of both INA analogues and SA derivatives to bind and inhibit tobacco catalase correlates with their biological activity to induce PR-1 gene expression and enhance resistance to tobacco mosaic virus. Comparison of the structures of INA, SA, and their anaslogues reveals several common features that appear to be important for biological activity. Thus, these results not only suggest that INA and SA share the same mechanism of action that involves binding and inhibition of catalase but also further indicate an important role for reactive oxygen species in the induction of certain plant defense responses. This is supported by the demonstration that INA-mediated PR-1 gene activation is suppressed by antioxidants.

Salicyclic acid (SA) is not a direct signal for the induction of catalase genes and requires other signals. Catalase is important for plants when stressed by elevated metabolic activities, such as during germination. Catalase helps to maintain normal cellular function and nullifies the toxic effects of hydrogen peroxide. SA has been thought to be a signal molecule by acting as a catalase inhibitor. The responses of three maize catalase genes, Cat1, Cat2 and Cat3, to SA was examined at embryogenesis and germination. Each catalase gens shows a unique germination related response to different doses of SA. During late embryogenesis, all catalase activity increased with 1mM SA treatment.

The metabolism of 5-aminosalicylate (5AS) in Pseudomonas sp. BN9 was described. Cell-free extracts from Pseudomonas sp. BN9 oxidized 5-AS to cis-4-amino-6-carboxy-2-oxo-hexa-3,5-dienoate (cis-ACOHDA). In the presence of glutathione, this ring-fission product is further degraded to L-malate, pyruvate and ammonia. Glutathione, light and acids also catalyse the spontaneous isomerization of cis-ACOHDA to its trans-isomer. The degradative pathway of 5AS converges at the fumarylpyruvate stage with the degradative pathway for gentisate.