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:

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SummaryDefence against pathogens in Arabidopsis is orchestrated by at least three signalling molecules: salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). The hrl1 (hypersensitive response-like lesions 1) mutant of Arabidopsis is characterized by spontaneous necrotic lesions, accumulation of reactive oxygen species, constitutive expression of SA-and ET/JA-responsive defence genes, and enhanced resistance to virulent bacterial and oomycete pathogens. Epistasis analyses of hrl1 with npr1, etr1, coi1 and SAdepleted nahG plants revealed novel interactions between SA and ET/JA signalling pathways in regulating defence gene expression and cell death. RNA gel-blot analysis of RNA isolated separately from the lesion + and the lesion ± leaves of double mutants of hrl1 revealed different signalling requirements for the expression of defence genes in these tissues. Expression of the ET/JA-responsive PDF1.2 gene was markedly reduced in hrl1 npr1 and in SA-depleted hrl1 nahG plants. In hrl1 nahG plants, expression of PDF1.2 was regulated by benzathiadiazole in a concentration-dependent manner: induced at low concentration and suppressed at high concentration. The hrl1 etr1 plants lacked systemic PR-1 expression, and exhibited compromised resistance to virulent Pseudomonas syringae and Peronospora parasitica. Inhibiting JA responses in hrl1 coi1 plants lead to exaggerated cell death and severe stunting of plants. Finally, the hrl1 mutation lead to elevated expression of AtrbohD, which encodes a major subunit of the NADPH oxidase complex. Our results indicate that defence gene expression and resistance against pathogens in hrl1 is regulated synergistically by SA and ET/JA defence pathways.

Experiments were conducted to determine how the timing of an exposure to ozone influenced the impact of the gas on ribulose-l,5-bisphosphate carboxylase/oxygenase (Rubisco) throughout the life span of a designated leaf. Saplings of Populus maximowizti x trichocarpa XE 388 received 5-d exposures to O^ in growth chambers during and at the termination of presumed synthesis of Rubisco in a designated leaf. Ozone had no detectable impact on Rubisco activity or quantity when the exposure occurred during the time of increasing concentration oi the protein in the leaf. When the concentration of Rubisco was near its peak, O^ induced a reduction in quantity and activity of Rubisco, but after cessation of the O^ stress, levels converged with those of the untreated tissue. When Og exposure occurred after full leaf expansion, minimal effects of the gas could be detected. When plants of hybrid popular or Raphanus sativus L. cv. Cherry Belle received chronic O3 treatment throughout the lifespan of the leaf, Rubisco activity and quantity' declined more rapidly and never converged with values of untreated tissue.Studies of gas exchange revealed that changes in Rubisco were associated with a decline in net photosynthesis (A) and that these effects preceded the observed reduction in foliar conductance. CO, response curves were measured periodically, and the initial slope (linear portion) of the curve, reflecting carboxylation capacity, declined more rapidly with leafage in O^-treated than in untreated poplars. There was no effect of O^ on stomatal limitation to COj assimilation except for a slight increase during the last 2 wk of the 9-wk experiment. This supported the hypothesis that O^ effects on A were associated with CO^-fixing capability of the leaf.