Salicylic acid (SA) is hypothesized to be a natural signal that triggers the systemic induction of pathogenesis-related proteins and disease resistance in tobacco. When Xanthi-nc (NN genotype) tobacco was inoculated with tobacco mosaic virus (TMV) there was an increase in endogenous SA in both inoculated and virus-free leaves. The highest levels of SA were detected in and around necrotic lesions that formed in response to TMV. Chemical and enzymatic hydrolysis of extracts from TMV-inoculated leaves demonstrated the presence of a SA conjugate tentatively identified as O-fi-Dglucosyl-SA. The SA conjugate was detected only in leaves that contained necrotic lesions and was not detected in phloem exudates or uninoculated leaves of TMV-inoculated Xanthi-nc tobacco. When exogenous SA was fed to excised tobacco leaves, it was metabolized within 10 hr. However, this reduction in free SA did not prevent the subsequent accumulation of the PR-1 family of pathogenesis-related proteins. The absence of SA accumulation in TMV-inoculated tobacco plants incubated at 32C was not a result of the glucosylation of SA. The addition of SA to the medium elevated levels of SA in the leaves of virus-free tobacco grown hydroponically. Increasing the endogenous level of SA in leaves to those naturally observed during systemic acquired resistance resulted in increased resistance to TMV, expressed as a reduction in lesion area. These data further support the hypothesis that SA is a likely natural inducer of pathogenesis-related proteins and systemic acquired resistance in TMV-inoculated Xanthi-nc tobacco.
Abstract.In tobacco (Nicotiana tabacum L. cv. Xanthinc), salicylic acid (SA) levels increase in leaves inoculated by necrotizing pathogens and in healthy leaves located above the inoculated site. Systemic SA increase may trigger disease resistance and synthesis of pathogenesis-related proteins (PR proteins). Here we report that ultraviolet (UV)-C light or ozone induced biochemical responses similar to those induced by necrotizing pathogens. Exposure of leaves to UV-C light or ozone resulted in a transient ninefold increase in SA compared to controls. In addition, in UV-light-irradiated plants, SA increased nearly fourfold to 0.77 lag'g ~ fresh weight in leaves that were shielded from UV light. Increased SA levels were accompanied by accumulation of an SA conjugate and by an increase in the activity of benzoic acid 2-hydroxylase which catalyzes SA biosynthesis. In irradiated and in unirradiated leaves of plants treated with UV light, as well as in plants fumigated with ozone, PR proteins l a and lb accumulated. This was paralleled by the appearance of induced resistance to a subsequent challenge with tobacco mosaic virus. The results suggest that UV light, ozone fumigation and tobacco mosaic virus can activate a common signal-transduction pathway that leads to SA and PR-protein accumulation and increased disease resistance. Key words:
Oxalate oxidase (OXO) converts oxalic acid (OA) and O 2 to CO 2 and hydrogen peroxide (H 2 O 2 ), and acts as a source of H 2 O 2 in certain plant-pathogen interactions. To determine if the H 2 O 2 produced by OXO can function as a messenger for activation of defense genes and if OXO can confer resistance against an OA-producing pathogen, we analyzed transgenic sunflower (Helianthus annuus cv SMF3) plants constitutively expressing a wheat (Triticum aestivum) OXO gene. The transgenic leaf tissues could degrade exogenous OA and generate H 2 O 2 . Hypersensitive response-like lesion mimicry was observed in the transgenic leaves expressing a high level of OXO, and lesion development was closely associated with elevated levels of H 2 O 2 , salicylic acid, and defense gene expression. Activation of defense genes was also observed in the transgenic leaves that had a low level of OXO expression and had no visible lesions, indicating that defense gene activation may not be dependent on hypersensitive response-like cell death. To further understand the pathways that were associated with defense activation, we used GeneCalling, an RNA-profiling technology, to analyze the alteration of gene expression in the transgenic plants. Among the differentially expressed genes, full-length cDNAs encoding homologs of a PR5, a sunflower carbohydrate oxidase, and a defensin were isolated. RNA-blot analysis confirmed that expression of these three genes was significantly induced in the OXO transgenic sunflower leaves. Furthermore, treatment of untransformed sunflower leaves with jasmonic acid, salicylic acid, or H 2 O 2 increased the steady-state levels of these mRNAs. Notably, the transgenic sunflower plants exhibited enhanced resistance against the OA-generating fungus Sclerotinia sclerotiorum.Oxidative burst, including hydrogen peroxide (H 2 O 2 ) production, is one of the early events that are associated with a hypersensitive response (HR) in many plant-pathogen interactions (HammondKosack and Jones, 1996; Lamb and Dixon, 1997). Several defensive roles for H 2 O 2 have been proposed (Lamb and Dixon, 1997). For example, H 2 O 2 in plant tissues may reach levels that are directly toxic to microbes (Peng and Kú c, 1992). H 2 O 2 may contribute to the structural reinforcement of plant cell walls (Bolwell et al., 1995) and trigger lipid peroxide and salicylic acid (SA) synthesis (Leô n et al., 1995). Moreover, H 2 O 2 appears to have roles in signal transduction cascades that coordinate various defense responses, such as induction of HR and synthesis of pathogenesis-related (PR) proteins and phytoalexins (Greenberg et al., 1994; Hammond-Kosack and Jones, 1996). These important roles of H 2 O 2 have attracted molecular pathologists' interest in manipulating the H 2 O 2 level by overexpressing an H 2 O 2 -generating enzyme, such as Glc oxidase (Wu et al., 1995; Kazan et al., 1998), to combat diseases in plants.Oxalate oxidase (OXO; EC 1.2.3.4) is one of the enzymes that can produce H 2 O 2 in plants. It releases CO 2 and H 2 O 2 from O 2...
Systemic induction of pathogenesis-related (PR) proteins in tobacco, which occurs during the hypersensitive response to tobacco mosaic virus (TMV), may be caused by a minimum 10-fold systemic increase in endogenous levels of salicylic acid (SA). This rise in SA parallels PR-1 protein induction and occurs in TMV-resistant Xanthi-nc tobacco carrying the N gene, but not in TMV-susceptible (nn) tobacco. By feeding SA to excised leaves of Xanthi-nc (NN) tobacco, we have shown that the observed increase in endogenous SA levels is sufficient for the systemic induction of PR-1 proteins. TMV infection became systemic and Xanthi-nc plants failed to accumulate PR-1 proteins at 32 degrees C. This loss of hypersensitive response at high temperature was associated with an inability to accumulate SA. However, spraying leaves with SA induced PR-1 proteins at both 24 and 32 degrees C. SA is most likely exported from the primary site of infection to the uninfected tissues. A computer model predicts that SA should move rapidly in phloem. When leaves of Xanthi-nc tobacco were excised 24 hr after TMV inoculation and exudates from the cut petioles were collected, the increase in endogenous SA in TMV-inoculated leaves paralleled SA levels in exudates. Exudation and leaf accumulation of SA were proportional to TMV concentration and were higher in light than in darkness. Different components of TMV were compared for their ability to induce SA accumulation and exudation: three different aggregation states of coat protein failed to induce SA, but unencapsidated viral RNA elicited SA accumulation in leaves and phloem. These results further support the hypothesis that SA acts as an endogenous signal that triggers local and systemic induction of PR-1 proteins and, possibly, some components of systemic acquired resistance in NN tobacco.
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