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

Background and objectives
We aim is to understand the mechanism(s) by which salicylic acid (SA), a natural inducer of plant resistance to pathogens, inhibits the movement of virus through host tissues. Recognition of a pathogen by a resistant plant sets in motion a sequence of events leading to biochemical and physiological changes in the plant that inhibit or eradicate the invading micro-organism, The resistance response in plants often takes the form of localised cell death at the site of pathogen entry (the hypersensitive response, HR) followed by a plant-wide induction of an enhanced resistance status (systemic acquired resistance, SAR). SA is a key component of the signal transduction pathway that leads from plant-pathogen recognition to the induction of the HR and SAR (1). Indeed, SA application to susceptible plants induces resistance to all three major classes of microbial plant pathogens, fungi, bacteria and viruses.

SA-responsive gene products have been identified. Some of them, particularly the pathogenesis-related (PR) proteins play important roles in defence. Although PR proteins have an established role against fungi and bacteria, there is no evidenoe that PRs mediate resistance to viruses (2).

Results and conclusions
It was recently demonstrated that SA treatment of susceptible tobacco tissue induced resistance to TMV by interfering with replication (3). In contrast to this we have shown that the replication of cucumber mosaic virus (CMV) in susceptible tobacco leaf discs is not affected by SA treatment. However, SA treatment of whole plants considerably delayed symptom development in CMV inoculated tobacco. These observations strongly suggest that SA was modifying the movement of CMV.
Western analysis of whole plants demonstrated that CMV exit from inoculated leaves was retarded in SA-treated plants, indicating an effect on long distance movement. Plant virus movement is known to parallel the translocation of photosynthates from source to sink leaves. l 4CO2-feeding experiments showed that SA treatment does not interfere with the movement of newly synthesised radiolabelled carbon compounds, nor change the boundary of the carbon sink/source transition in young expanding leaves. Thus SA-induced inhibition of long-distance movement is not due to perturbation of carbohydrate translocation. Experiments are in progress to examine virus entry into sieve elements in order to identify which cell-types act as barriers to CMV movement in SA treated plants Recently, it was reported that SA interference of TMV replication is induced via a novel branch of the defensive signal transduction pathway that is sensitive to salicylihydroxamic acid (SHAM; 3). Surprisingly, SA-induced resistance to CMV was also abolished by SHAM, implicating the SHAM-sensitive signalling pathway in the activation of the mechanism(s) underlying inhibition of virus long-distance movement.

1. Malamy J, Carr JP, Klessig DF, Raskin I, 1990. Science 250,1002-1004.
2. CuttJ R, HarpsterMH, Dixon DC, Carr JP, Dunsmuir P, Klessig DF, (1989). Virology 173, 89-97
3. Chivasa S, Murphy AM, Naylor M, Carr JP, 1997. Plant Cell 9, 547-557.