Phenolic biosynthesis inhibitors suppress adult plant resistance toErysiphe graminisin oat at 20 °C and 10 °C

Seedling and adult plant leaves of three oat genotypes, Selma, Maldwyn and OM1387 (a hybrid derived from a Selma×Maldwyn cross), were excised and treated with water or with α-amino-β-phenylpropionic acid (AOPP) to inhibit phenylalanine ammonia lyase activity, or with [[(2-hydroxyphenly)amino] sulfinyl]acid 1,1-dimethylethyl ester (OH-PAS) to inhibit cinnamyl alcohol dehydrogenase activity. None of these genotypes possess any known major gene resistance to the isolate ofErysiphe graminisf.sp.avenaewith which they were inoculated, although Maldwyn is known to possess quantitative adult plant resistance that has proved durable since 1947. All genotypes showed some adult plant resistance which limited the proportion of fungal appressoria that formed haustoria in water-treated leaves. However, this resistance was expressed more strongly in Maldwyn and OM1387 than in Selma. Treatment with AOPP or OH-PAS increased substantially the proportion of fungal appressoria that formed haustoria in adult as well as seedling leaves, indicating that phenolic compounds, probably products of the lignin biosynthetic pathway, contributed to resistance. However, AOPP-treated adult leaves remained more resistant to infection than AOPP-treated seedling leaves, suggesting that additional unknown factor(s) contributed to adult plant resistance. In all genotypes and in seedling and adult leaves, failure of appressoria to infect was correlated to the localized accumulation of autofluorescent components in host cell papillae and cell wall regions subtending appressoria. This localized autofluorescence was suppressed by AOPP treatment, and to a lesser extent by OH-PAS treatment, indicating that the fluorogens were phenolic compounds. In Maldwyn and OM1387 a proportion of host cells showed whole-cell autofluorescence, probably indicative of cell death, following attack by appressoria. Whole-cell autofluorescence was almost totally suppressed by AOPP or OH-PAS treatment, suggesting that this response was also dependent upon active synthesis of phenolic compounds. The contribution of phenolic compound synthesis to disease resistance appeared to be independent of temperature; AOPP treatment had similar effects in suppressing resistance in plants acclimated and incubated at 10 °C and at 20 °C.