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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.

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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New Brunswick, New Jersey 08903-0231 (P.S., I.R.)Defense responses mediated by the genetically unlinked Cf-9 and Cf-2 genes were compared with those involving no Cf gene (CfO). Compatible tomato (Lycopersicon esculentum)-Cladosporiom fulvum intercellular washing fluids were injected into tomato cotyledons, and the kinetics of responses was monitored under conditions of 70 and 98% relative humidity. l h e latter conditions suppressed the normal macroscopic responses. For the Cf-9-Avr9 interaction, stomatal opening was induced within 3 to 4 h and after 9 h mesophyll cell death commenced. A burst of ethylene production occurred between 9 and 12.5 h and remained elevated. Free salicylic acid levels increased after 12 h, peaked at 24 h, and thereafter declined. For the Cf-2-Avr2 interaction, stomata became plugged after 8 h, and salicylic acid and ethylene levels increased by 12 and 1 8 h, respectively, and thereafter declined. Host cell death commenced around vascular tissue by 24 h. Cell death in both incompatible interactions was frequently preceded by cell enlargement. For CfO-injected plants, no significant responses were detected. High humidity delayed and reduced the Cf-Avr-gene-dependent cell death and ethylene synthesis, whereas induced salicylic acid levels were unaffected for Cf-2-Avr2 and reduced in magnitude only for Cf-9-A vr9.An array of highly localized plant defenses are induced rapidly and coordinately at the site of genetically incompatible plant-pathogen interactions. Subsequently, the growth of the invading virus, bacteria, fungus, or nematode is retarded, and eventually the microbe either dies or remains quiescent. Activation of localized plant defenses is dependent on mutual recognition between plant and microbe. This recognition is hypothesized to result from the interaction of the product of a dominant or semidominant

Jersey 08903-0231 (P. Silverman, M.S., I.R.)The possible role of the octadecanoid signaling pathway with jasmonic acid (JA) as the central component i n defense-gene regulation of pathogen-attacked rice was studied. Rice (Oryza sativa 1.) seedlings were treated with JA or inoculated with the rice blast fungus Magnaporthe grisea (Hebert) Barr., and gene-expression patterns were compared between the two treatments. JA application induced the accumulation of a number of pathogenesis-related (PR) gene products at the mRNA and protein levels, but pathogen attack did not enhance the levels of (-)-JA during the time required for PR gene expression. Pathogen-induced accumulation of PR1 -like proteins was reduced in plants treated with tetcyclacis, a nove1 inhibitor of jasmonate biosynthesis. There was an additive and negative interaction between JA and an elicitor from M. grisea with respect to induction of PR1-like proteins and of an abundant JA-and wound-induced protein of 26 kD, respectively. Finally, activation of the octadecanoid signaling pathway and induction of a number of PR genes by exogenous application of JA did not confer local acquired resistance t o rice. The data suggest that accumulation of nonconjugated (-)-JA is not necessary for induction of PR genes and that JA does not orchestrate localized defense responses in pathogen-attacked rice. Instead, JA appears to be embedded in a signaling network with another pathogen-induced pathway(s) and may be required at a certain minimal leve1 for induction of some PR genes.The plant-growth regulator JA, first described as the methyl ester MeJA in the essential oils of Jasminum (Demole et al., 1962), has been attributed to a number of regulating functions in plant development (for review, see Sembdner and Parthier 119931). Only recently has attention been paid to jasmonates as the key molecules of the octadecanoid signaling pathway mediating the activation of defense responses in herbivore-or pathogen-attacked plants (for review, see Sembdner and Parthier [1993], Farmer [1994], and Creelman and Mullet [1995]). The wound and pathogen

The anemia associated with malaria is complex, and multiple factors contribute to its severity. An increased destruction and a decreased production of erythrocytes are involved; however, the mechanisms responsible remain unclear. Tumor necrosis factor alpha (TNF-a), released by macrophages in response to infection, is thought to play a role through its ability to inhibit erythropoiesis. In these studies we have examined erythropoiesis in mice infected with Plasmodium berghei and in mice infused with recombinant TNF-a via implanted osmotic pumps. In both groups of mice there was (i) a reduction of pluripotent stem cells in the bone marrow and a concomitant increase in the spleen, (ii) a reduction of erythroid progenitor cells, and (iii) a reduced incorporation of 59Fe into erythrocytes. When P. berghei-infected mice were given antiserum against recombinant murine TNF, erythropoiesis was partially restored. There was a significant increase in bone marrow stem cells, erythroid progenitor cells, and 59Fe incorporation into erythrocytes in P. berghei-infected mice that had been treated with anti-TNF. How TNF may act, directly or indirectly, to inhibit erythropoiesis is not yet clear. These results demonstrate that TNF mediates, in part, the anemia associated with malaria.