SALICYLATE-INDEPENDENT LESION FORMATION IN ARABIDOPSIS LSD MUTANTS

In many interactions of plants with pathogens, the primary host defens e reaction is accompanied by plant cell death at the site of infection . The resulting lesions are correlated with the establishment of an in ducible resistance in plants called systemic acquired resistance (SAR) , for which salicylic acid (SA) accumulation is a critical signaling e vent in Arabidopsis and tobacco, In Arabidopsis, the lesions simulatin g disease (lsd) mutants spontaneously develop lesions in the absence o f pathogen infection, Furthermore, lsd mutants express SAR marker gene s when lesions are present and are resistant to the same spectrum of p athogens as plants activated for SAR by necrogenic pathogen infection, To assess the epistatic relationship between SA accumulation and cell death, transgenic Arabidopsis unable to accumulate SA due to the expr ession of the salicylate hydroxylase (nahG) gene were used in crosses with the dominant mutants lsd2 or lsd4, Progeny from the crosses were inhibited for SAR gene expression and disease resistance, However, the se progeny retained the spontaneous cell death phenotype similar to si blings not expressing nahG. Because lesions form in the absence of SA accumulation for lsd2 and lsd4, a model is suggested in which lesion f ormation in these two mutants is determined prior to SA accumulation i n SAR signal transduction, By contrast, the loss of SAR gene expressio n and disease resistance in nahG-expressing lsd mutants indicates that these traits are dependent upon SA accumulation in the SAR signal tra nsduction pathway.