VIEW ARTICLE

Physiology and Biochemistry

Induction of Systemic Resistance to Anthracnose in Cucumber by Phosphates. Hans D. Gottstein, Department of Plant Pathology, University of Kentucky, Lexington, KY 40546-0091, Current address: Institute of Plant Biochemistry of the Academy of Sciences of the German Democratic Republic, Halle 4050, Weinberg 3 GDR; Joseph A. Kuc, Department of Plant Pathology, University of Kentucky, Lexington, KY 40546-0091. Phytopathology 79:176-179. Accepted for publication 19 August 1988. Copyright 1989 The American Phytopathological Society. DOI: 10.1094/Phyto-79-176.

Solutions of K₃PO₄, K₂HPO₄, NA₃PO₄, and NA₂HPO₄ sprayed on the undersides of the first and second true leaves of cucumber induced systemic resistance in leaves 3 and 4 to anthracnose caused by Colletotrichum lagenarium. Solutions of KH₂PO₄, NAH₂PO₄, CaHPO₄, (NH₄)₂ HPO₄, and NH₄H₂PO₄ were less active, and a suspension of Ca₃PO₄ was inactive. Induced resistance in leaves 3 and 4 depended on the concentration of K₃PO₄ applied to leaves 1 and 2. Spraying leaves 1 and 2 each with 1-2 ml of a solution of K₃PO₄ at concentrations of 100, 50, 10, 5, and 1 mM protected leaves 3 and 4 99, 96, 78, 54, and 15%, respectively. The level of protection was based on the total necrotic lesion area of plants sprayed on leaves 1 and 2 with water. A pH greater than 7.0 was required for high activity of potassium phosphates, and activity of di-and tripotassium phosphates was markedly reduced at lower pHs. Induction of systemic resistance, however, was not solely a result of an alkaline pH, because 50 mM potassium hydroxide (pH 11.7) was inactive. Induced systemic resistance was associated with the gradual appearance of chlorotic and necrotic stippling on leaves 1 and 2. The lack of stippling or rapid death of leaves 1 and 2 was associated with little or no induced systemic resistance. Induced systemic resistance in newly developing leaves above leaves 3 and 4 was apparent for at least 5 wk in greenhouse and outdoor tests. These data suggest that induced systemic resistance to disease caused by infection is not due to a specific component of the pathogen, but rather to the persistence of a low level of metabolic perturbation. One cause of such perturbation may be the sequestering of calcium ions.