A 90 kDa protein elicitor, PB90, was purified from the culture filtrate of Phytophthora boehmeriae. Procedures including hydrophobic interaction and ion-exchange chromatography were used to purify the protein. PB90 induced hypersensitive reaction in tobacco leaves at a concentration as low as 200 pM and induced systemic acquired resistance (SAR) to TMV, Alternaria alternata, P. parasitica and Ralstonia solanacearum. In addition, it also caused hypersensitive necrosis in leaves of Chinese cabbage and induced SAR to Collectorium higginsianum in the plant. Tobacco leaves infiltrated with 200 pM of the elicitor exhibited an enhanced phenylalanine ammonia lyase activity and peroxidase activity. The behavior on ion-exchange columns indicated that PB90 is an acidic protein. It is stable to heat, acidic and alkaline conditions, but sensitive to ProteaseK. An antiserum raised against the pure protein allowed localization of PB90 by immunogold labeling on the cell wall of the mycelia and encysting zoospores when the fungus is grown in vitro. It was implied that there is a novel protein elicitor secreted by P. boehmeriae, which has a broad activity spectrum. The characters of PB90 distinguished it clearly from the other elicitors previously identified from Phytophthora spp. The possible implications of such a novel elicitor in plant–microbe interactions are discussed.

We examined the role of salicylic acid (SA) accumulation in the tobacco hypersensitive response (HR) and systemic acquired resistance (SAR) induced by PB90, a 90 kDa protein elicitor that is secreted by Phytophthora boehmeriae. The elicitor induced HR of a consistent shape and size on tobacco plants expressing the bacterial gene nahG. Salicylate hydroxylase is encodec by nahG and inactivates SA by converting it into catechol. The mutant NahG does not accumulate SA. In contrast, infiltration with of a wild type tobacco (cv. Xanthi nc) leaves with the elicitor caused the increase of SA levels. The same SA levels were observed in leaves not treated by the elicitor. HR appears to be mediated by a SA-independent signaling pathway. PB90 treatment resulted in enhanced resistance of wild-type plants to infection by black shank fungus, P. nicotianae, and TMV, but not in NahG plants. Moreover, the elicitor-induced expression of an SAR marker gene encoding PR-1a was suppressed in NahG plants. These results indicate that SA mediates SAR but not HR in tobacco treated with PB90. During plant-elicitor interactions, HR and SAR may be regulated by distinct signal pathways, or SA may function as an intermediate signal upstream of SAR but downstream of HR, and HR may not be a direct defense mechanism against pathogen infection.