Relationship Between Localized Acquired Resistance (LAR) and the Hypersensitive Response (HR): HR Is Necessary for LAR to Occur and Salicylic Acid Is Not Sufficient to Trigger LAR

Abstract

In tobacco plants reacting hypersensitively to pathogen infection, localized acquired resistance (LAR) is induced in a sharp zone surrounding hypersensitive response (HR) lesions. Using a fungal glycoprotein inducing HR and LAR when infiltrated at 50 nM into tobacco leaves, we have shown previously that a plant signal(s) is released by HR cells and diffuses to induce LAR. Here we address two questions: does LAR occur when HR is not induced, and is salicylic acid the (or one of the) mobile LAR signal? We found that application to tobacco leaves of 0.25 nM glycoprotein triggered defense responses without HR and without an H₂O₂ burst. The analyzed responses include changes in expression of O-methyltransferase (OMT), 3-hydroxy-3-methylglutarylCoA reductase, pathogenesis-related (PR) proteins, and changes in levels of the signal salicylic acid. No defense responses and no increased resistance to tobacco mosaic virus infection were found beyond the elicitor-infiltrated tissue, providing strong evidence that there is no LAR without HR. Treatments of NahG tobacco leaves with 50 nM elicitor induced the HR and, in the sharp zone surrounding the HR lesion, a strong activation of OMT and of basic PR proteins, but not of acidic PR-1 proteins. This indicates that a signal different from salicylic acid is diffusing.