Abstract
Systemic acquired resistance (SAR) is a pathogen-inducible defense mechanism effective against a wide range of pathogens. Salicylic acid (SA) is an essential component of this pathway, as transgenic plants unable to accumulate salicylic acid are incapable of developing SAR. Here, we show that the synthetic chemical 2,6-dichloroisonicotinic acid (INA) acts via the SAR signal transduction pathway. However, it does not induce SA accumulation during the time required for the induction of SAR gene expression or resistance to TMV. Furthermore, INA can induce both resistance and SAR gene expression in transgenic tobacco and Arabidopsis plants that cannot accumulate SA. Thus, INA apparently activates a component of the SAR signaling pathway downstream of SA accumulation
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