Abstract: Elicitin is an extracellular elicitor protein form Phytophthora species induced hypersensitive response in the genus Nicotiana. A cDNA with length of 357 bp encoding capsicin, was amplified from Phytophthora capsici by reverse transcript PCR (RT-PCR) based on high homology of elicitin genes from various Phytophthora spp. The gene codes a predicted 118 amino acids protein containing a 20-amino acid signal peptide of that is processed before secretion and with a calculated pI of 4.2. By compared with published 14 elicitin sequences of Phytophthhora spp in Genbank, capsicin belongs to α-elicitin. Southern blot analysis indicated that capsicin genes occur at least two copies in P. capsici. Bacterial expression of the cloned elicitin gene as translational funsion protein yielded a biologically active protein capable of inducing a hypersensitive response in wile-type tobacco, suggesting that Phytophthora-specific posttranslational modifications of elicitin are not required for its activity. 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. HR appears to be mediated by a SA-independent signaling pathway. And elicitin treatment resulted in enhanced resistance of wild-type tobacco plants to infection by black shank fungus, P. nicotianae, and TMV. And the capsicin could induce 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 capsicin. 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.

Key words: Phytophthora capsici, elicitin, hypersensitive response, systemic acquired resistance