Recent advances in systemic acquired resistance research — a review

Genetic Dissection of Acquired Resistance to Disease

“…Those efforts resulted in the discovery of the SAR-activating compounds INA and BTH (Métraux et al, 1991;Gorlach et al, 1996), which induce the same set of genes and produce the same spectrum of resistance to disease as found in biologically induced SAR, supporting the proposed mode of action of these chemicals through induction of the SAR pathway (Kessmann et al, 1994). It is interesting that INA and BTH can induce resistance in plants that are unable to accumulate SA because of expression of salicylate hydroxylase, showing that the site of activity for these chemicals is either at or downstream from the site of SA action in the signal transduction pathway leading to SAR (Delaney et al, 1994b;Vernooij et al, 1995;Lawton et al, 1996).…”

“…This view is supported by the finding that niml plants retain the ability to accumulate SA in response to pathogens and yet cannot respond to this signal . By contrast, whereas lsd, cprl, and cim mutants show constitutive activation of the SAR pathway and exhibit elevated SA levels, depletion of SA by nahG expression suppressed SAR gene expression and resistance phenotypes in all lines examined (Bowling et al, 1994;Weymann et al, 1995;Hunt et al, 1996). These observations indicate that the lsd, cprl, and cim mutations tested are disrupted upstream of SA in the signaling pathway.…”

“…The simultaneous occurrence of HR-like lesions and Dietrich et al, 1994Weymann et al, 1995Greenberg et al, 1994 Activation of defense pathways in the absence of a 1. hypersensitive cell death lesions 2. SAR SA removal shown to suppress lesion formation in lsd6 and Isd7 but not in lsd2 or lsd4 Hunt et al, 1996) pathogen trigger, causing expression of: (Dietrich et al, 1994), lsd6, and lsd7 and (accelerated cell __ death-2) acd2 (Greenberg et al, 1994) mutants. These lines were identified by their visible lesion phenotype (lsdl, lsd3, Isd4, and lsd5), their constitutive high-leve1 expression of SAR genes (lsd2, Isd6, and lsd7), or their propensity to form HR lesions following inoculation with virulent Pst strains (acd2).…”

“…The N I M l gene product may act as an SA receptor, provided that it also interacts with INA and BTH, since each of these SAR-inducing chemicals fails to function in niml mutants Lawton et al, 1996). Alternatively, the NIMl gene product may act downstream of reception of the SA, INA, and BTH signals.…”

“…Although nahG expression suppressed SAR gene activation and resistance phenotypes in all lines, striking differences were observed in the expression of the lesion phenotype. Upon introduction of the salicylate hydroxylase gene, lsd2 and lsd4 lines maintained their lesion-forming phenotype (Hunt et al, 1996), whereas lsd6 and lsd7 lines showed NahG suppression of lesion formation. It is interesting that the suppression of lesions observed in lsd6 / NahG plants could be reversed by Genetic Analysis of lnduced Resistance 9 application of INA or SA .…”