Inoculation of one true leaf of cucumber (Cucumis sativus L.) plants with Pseudomonas syringae pathovar syringae results in the systemic appearance of salicylic acid in the phloem exudates from petioles above, below, and at the site of inoculation. Analysis of phloem exudates from the petioles of leaves 1 and 2 demonstrated that the earliest increases in salicylic acid occurred 8 hours after inoculation of leaf 1 in leaf 1 and 12 hours after inoculation of leaf 1 in leaf 2. Detaching leaf I at intervals after inoculation demonstrated that leaf I must remain attached for only 4 hours after inoculation to result in the systemic accumulation of salicylic acid. Because the levels of salicylic acid in phloem exudates from leaf I did not increase to detectable levels until at least 8 hours after inoculation with P. s. pathovar syringae, the induction of increased levels of salicylic acid throughout the plant are presumably the result of another chemical signal generated from leaf I within 4 hours after inoculation. Injection of salicylic acid into tissues at concentrations found in the exudates induced resistance to disease and increased peroxidase activity. Our results support a role for salicylic acid as an endogenous inducer of resistance, but our data also suggest that salicylic acid is not the primary systemic signal of induced resistance in cucumber.Inoculation of one leaf of cucumber plants and other cucurbits with necrotic lesion-inducing pathogens (7-9) or necrosis/chlorosis-inducing chemicals (3, 4) results in the expression of systemic resistance against disease caused by a number of pathogens. The onset of resistance has been correlated with the initial appearance of necrotic lesions and generally begins to develop 3 to 4 d after the resistance-inducing inoculation (7-9).We have recently demonstrated that systemic resistance can be induced in cucumber within 24 h by inoculating leaf with the HR2-inducing bacterium Pseudomonas syringae pv syringae (17 demonstrated that this leaf must remain attached for only 6 h to result in the systemic expression of enhanced peroxidase activity and a small, but detectable, increase in the level of systemic disease resistance. Allowing the first leaf to remain on the plant for up to 12 h after inoculation with P. s. pv syringae resulted in a further increase in the level of systemic resistance as compared with plants that had the inoculated first leaf detached 6 h after inoculation. TnS mutants of P. s. pv syringae that had lost the ability to induce the HR were also unable to induce systemic resistance and peroxidase activity.Dean and Kuc (1, 2) have provided strong evidence that the systemic signal(s) for induced resistance was generated in and mobilized out of the leaves that were initially inoculated ("source" leaves) with resistance-inducing pathogens. Metraux et al. ( 12) recently reported that cucumber plants inoculated with either Colletotrichum lagenarium or tobacco necrosis virus on one leaf had higher levels of salicylic acid (an exogenous inducer ofres...

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The principal phytoalexin that accumulates i n Arabidopsis fbaliana after infection by fungi or bacteria is 3-thiazol-2'-yl-indole (camalexin). Many plant species produce antimicrobial compounds, known as phytoalexins, after pathogen infection. In general, members of a particular plant family will produce phytoalexins that belong to the same class of compounds (Bailey and Mansfield, 1982). Leguminous plants produce isoflavanoid and/ or pterocarpan phytoalexins, whereas solanaceous plants produce sesquiterpenoid phytoalexins. AI1 of the phytoalexins that have been characterized from the members of the Brassicaceae are indole derivatives that are substituted at the C-3 position with a sulfur-containing moiety (Hammerschmidt et al., 1993). Conn et al. (1988) reported that Cumelina sativa (false flax) accumulated two different phytoalexins after infection with Alternaria brassicae, a funga1 pathogen of rapeseed. The most abundant of the two phytoalexins was identified

We are working to determine the role of the Arabidopsis phytoalexin, camalexin, in protecting the plant from pathogen attack by isolating phytoalexin-deficient (pad) mutants in the accession Columbia (Col-0) and examining their response to pathogens. Mutations in PAD1, PAD2, and PAD4 caused enhanced susceptibility to the bacterial pathogen Pseudomonas syringae pv. maculicola strain ES4326 (PsmES4326), while mutations in PAD3 or PAD5 did not. Camalexin was not detected in any of the double mutants pad1-1 pad2-1, pad1-1 pad3-1 or pad2-1 pad3-1. Growth of PsmES4326 in pad1-1 pad2-1 was greater than that in pad1-1 or pad2-1 plants, while growth in pad1-1 pad3-1 and pad2-1 pad3-1 plants was similar to that in pad1-1 and pad2-1 plants, respectively. The pad4-1 mutation caused reduced camalexin synthesis in response to PsmES4326 infection, but not in response to Cochliobolus carbonum infection, indicating that PAD4 has a regulatory function. PAD1, PAD2, PAD3 and PAD4 are all required for resistance to the eukaryotic biotroph Peronospora parasitica. The pad4-1 mutation caused the most dramatic change, exhibiting full susceptibility to four of six Col-incompatible parasite isolates. Interestingly, each combination of double mutants between pad1-1, pad2-1 and pad3-1 exhibited additive shifts to moderate or full susceptibility to most of the isolates.