Induction of systemic acquired resistance in cucumber by Pseudomonas syringae pv. syringae 61 HrpZPss protein

Published

Journal Article

Systemic acquired resistance (SAR) is an inducible plant defense response and is effective against a broad spectrum of pathogens. Biological induction of SAR usually follows plant cell death resulting from the plant hypersensitive response (HR) elicited by an a virulent pathogen or from disease necrosis caused by a virulent pathogen. The elicitation of the HR and disease necroses by pathogenic bacteria is controlled by hrp genes. Previously, it was shown that the Pseudomonas syringae 61 (Pss61) HrpZPss protein (formally harpinPss) elicited the HR in plants. In this study, it is shown that HrpZpss induced SAR in cucumber to diverse pathogens, including the anthracnose fungus (Colletotrichum lagenarium), tobacco necrosis virus and the bacterial angular leaf spot bacterium (P. s. pv. lachrymans). A hrpH mutant of Pss61, which is defective in the secretion of HrpZPss and, possibly, other protein elicitors, failed to elicit SAR. Pathogenesis-related (PR) proteins, including peroxidase, β-glucanase and chitinases, were induced in cucumber plants inoculated with Pss61, C. lagenarium or HrPZpss. The induction patterns of PR proteins by HrpZPss and Pss61 were the same, but were different from that induced by C. lagenarium. Interestingly, the hrpH mutant induced two of the three identified PR proteins, despite its failure to induce SAR. These results suggest that proteinaceous elicitors, such as HrPZPss, that traverse the bacterial Hrp secretion pathway are involved in the biological induction of SAR and that at least some PR proteins can be induced by bacterial factors that are not controlled by hrp genes.

Full Text

Duke Authors

Cited Authors

  • Strobel, NE; Ji, C; Gopalan, S; Kuc, JA; He, SV

Published Date

  • January 1, 1996

Published In

Volume / Issue

  • 9 / 4

Start / End Page

  • 431 - 439

International Standard Serial Number (ISSN)

  • 0960-7412

Digital Object Identifier (DOI)

  • 10.1046/j.1365-313X.1996.09040431.x

Citation Source

  • Scopus