Delayed inducible resistance (DIR) is triggered by artificial or herbivore—caused foliar damage and is manifested as decreased performance of herbivore generation(s) feeding on the trees subsequent to the generation during which the damage took place. DIR is associated with increase in concentrations of foliage phenolics and decrease in nitrogen. The growth—differentiation balance hypothesis, and the carbon—nutrient balance (CNB) hypothesis contained in it, claim that DIR is caused by nutritional stress after defoliation of trees growing on nutrient—poor soils. In these environments, nutrient uptake limits plant growth more strongly than does photosynthesis; that is, carbon—based secondary metabolites (e.g., phenolics) are prone to accumulate. According to the CNB hypothesis, an excess of limiting nutrient(s) or reduced photosynthetic rate should lead to elimination of DIR. We tested this using same—aged Betula pubescens ssp. tortuosa trees of five open—pollinated families growing in a common arboretum in northernmost Finland. In addition to unmanipulated control trees, we had three nutritional treatments during three successive growth seasons: N—fertilization, PK—fertilization adding all nutrients except N, and shading to decrease carbon assimilation. Half of the trees in each treatment were artificially defoliated (50% leaf area) in the second study year, one year before the growth trial with geometrid (Epirrita autumnata) larvae. Tree growth measurements showed that N is the growth—limiting nutrient in our study area. N—fertilization and shading of the trees affected foliage chemistry generally as proposed by the CNB hypothesis. For example, they reduced foliar concentrations of total phenolics and condensed tannins. The birch families differed significantly in foliage chemistry, suggesting genetic differences, but the differences were not associated with fertilizations, shading, or defoliation of the trees. Contrary to fertilizing—shade treatments, changes in leaf chemistry and E. autumnata performance caused by defoliation were not consistent with the CNB hypothesis. For example, defoliation caused significant DIR irrespective of N—fertilization or shading. There were no significant differences among the birch families in performance of the moth larvae or in effects of fertilization, shade, or defoliation on larval performance. These responses to defoliation contrast with those of some other studies, especially those on the Betula resinifera—Rheumaptera hastata system in Alaska, which provide clear support for the CNB as an explanation of DIR. We find methodological differences to be an unlikely explanation for the different results but are unable to propose any single mechanism that will explain the diverse plant responses.
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