October 1991 | Eric R. Ward, Scott J. Uknes, Shericca C. Williams, Sandra S. Dincher, Deanna L. Wiederhold, Danny C. Alexander, Patricia Ahl-Goy, Jean-Pierre Métraux, and John A. Ryals
The study investigates the molecular basis of systemic acquired resistance (SAR) in tobacco, a phenomenon where plants develop a generalized resistance to pathogens after initial infection. The authors identify nine gene families that are coordinately induced during the onset of SAR. These genes, referred to as SAR genes, include various pathogenesis-related (PR) proteins and enzymes such as chitinases and β-1,3-glucanases. The induction of these genes is correlated with the development of SAR, as evidenced by the reduction in lesion size caused by subsequent infections. Salicylic acid (SA), a candidate endogenous signal, and methyl-2,6-dichloroisonicotinic acid (INA), a synthetic immunization compound, were found to induce the same set of SAR genes. The results suggest that SAR is partially or fully dependent on the coordinated expression of these genes. The study also proposes a model linking pathogen-induced necrosis to the biosynthesis of SA and the induction of SAR.The study investigates the molecular basis of systemic acquired resistance (SAR) in tobacco, a phenomenon where plants develop a generalized resistance to pathogens after initial infection. The authors identify nine gene families that are coordinately induced during the onset of SAR. These genes, referred to as SAR genes, include various pathogenesis-related (PR) proteins and enzymes such as chitinases and β-1,3-glucanases. The induction of these genes is correlated with the development of SAR, as evidenced by the reduction in lesion size caused by subsequent infections. Salicylic acid (SA), a candidate endogenous signal, and methyl-2,6-dichloroisonicotinic acid (INA), a synthetic immunization compound, were found to induce the same set of SAR genes. The results suggest that SAR is partially or fully dependent on the coordinated expression of these genes. The study also proposes a model linking pathogen-induced necrosis to the biosynthesis of SA and the induction of SAR.