Fosetyl-Al alters the respiratory response in Phytophthora nicotianae var. nicotianae-infected tobacco

Abstract

Inoculation of susceptible 21-day-old tobacco (cv. 26T68) seedlings by zoospores of the black shank fungus ( Phytophthora nicotianae var. nicotianae) is followed by rapid colonization, cellular degradation and metabolic disruption. Oxygen consumption increases rapidly in the first 13 h after inoculation from 15·3 μmol g −1 h −1 to 31·4 μmol g −1 h −1. By 33 h after inoculation, sporangia have formed profusely, and oxygen consumption rises further to 52·9 μmol g −1 h −1. Up to 12 h after inoculation glycolysis is regulated by pyruvate kinase. After 18 h glycolysis is unregulated. In seedlings protected by 282 μ m fosetyl-Al (aluminium tris ( o-ethylphosphonate)) oxygen consumption rises 7 h after inoculation from a higher initial rate than in untreated seedlings, 19·7 μmol g −1 h −1, to 30·0 μmol g −1 h −1, then falls to 12·9 μmol g −1 h −1 at 15 h. By 33 h after inoculation it has risen again to 37·9 μmol g −1 h −1. This pattern resembles that in a resistant cv., NC 2326. In cv. 26T68 seedlings treated with fosetyl-Al glycolysis remains under the control of phosphofructokinase, and ADP and ATP levels are relatively constant, reflecting only minor disturbances to cellular integrity resulting from the restricted fungal growth. Coinciding with the drop in oxygen consumption between 9 and 15 h after inoculation is a rapid rise in the level of 6-phosphogluconate, indicating a diversion of glycolysis to pentose phosphate metabolism. These observations add to the evidence that changes in the host response to infection are involved in the mode of action of fosetyl-Al.