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.