Exogenous spermidine, arsenic and beta-aminobutyric acid modulate tobacco resistance to tobacco mosaic virus, and affect local and systemic glucosylsalicylic acid levels and arginine decarboxylase gene expression in tobacco leaves.

The polyamine spermidine and the metalloid arsenic increased resistance responses in the well-known pathosystem NN tobacco/tobacco mosaic virus (TMV). Both the hypersensitive response to TMV in a leaf disk model system (inoculated disks floating in the 0.1mM treatments) and systemic acquired resistance (SAR) in whole plants were significantly affected. In the latter case, 1mM foliar sprays of spermidine and arsenic were as effective as TMV and dl-beta-aminobutyric acid (BABA), both taken as positive controls, in improving the plant's response to subsequent challenge inoculation with TMV. Moreover, this phenotypic response was correlated with changes in the endogenous concentration of the SAR-related molecule salicylic acid and in transcript levels of some pathogenesis/stress-related genes (pathogenesis-related proteins PR-1a and PR-2 and arginine decarboxylase (ADC)). Concentrations of free salicylic acid and of 2-O-beta-d-glucosylsalicylic acid and mRNA amount of PR-1a, PR-2 and ADC were analyzed in plants treated with either spermidine or arsenic, and compared with those from untreated plants and from positive (TMV-inoculated or BABA-treated) controls. Conjugated salicylic acid content and ADC transcripts were found to significantly increase, at both the local and systemic levels, relative to untreated controls.