1.4.37
THE EFFECT OF SALICYLIC ACID ON CAULIFLOWER MOSAIC VIRUS

RAJ CARSON and JP CARR

Department of Plant Sciences, Cambridge University, Downing Street, Cambridge CB2 3EA, UK

Background and objectives
Pathogen recognition in disease-resistant plants can result in localized cell death around the site of infection (the hypersensitive response) and a heightened resistance response to further pathogen attack (systemic acquired resistance; SAR). Salicylic acid (SA) plays a vital role in the signal transduction pathway that leads to the establishment of SAR. SA-induced pathogenesis-related proteins contribute to fungal and bacterial resistance, but the mechanism by which SA mediates viral resistance has not been fully characterized. Recent studies have examined the effect of SA on the replication of viruses with single-stranded, positive-sense RNA genomes. SA inhibited tobacco mosaic virus [1] and potato virus X replication and cucumber mosaic virus movement (Naylor M et al., in preparation). SA induced both of these resistance mechanisms via a novel signal transduction pathway that could be inhibited by salicyihydroxamic acid (SHAM). We wanted to discover what effect SA would have on the replication or movement of a virus with a DNA genome.

Results and conclusions
Experiments were conducted using cauliflower mosaic virus (CAMV) which has a dsDNA genome and replicates via an RNA intermediate. Application of SA to Arabidopsis plants for 4 days prior to inoculation delayed symptom development by up to 5 days compared with water controls. Symptoms began to develop as early as 9 days post-inoculation (d.p.i.) in the controls, but consistently did not appear until 14 d.p.i. in SA-treated plants. Western blotting revealed a complete supression of coat protein (CP) accumulation in SA-treated plants at 13 d.p.i., and even by 17 d.p.i. CP levels were still lower than water controls. Experiments are in progress to examine the effect of SA on CAMV DNA and RNA accumulation as well as virus movement. We are also in the process of determining whether SA-induced resistance to CAMV is mediated via the SHAM-sensitive signal-transduction pathway.

References
1. Chivasa S, Murphy AM, Naylor M, Carr JP, 1997. Plant Cell 9, 547-557.