Effects of Mineral Nutrition on Delayed Inducible Resistance in Alaska Paper Birch

Abstract

In subarctic forests, birch (Betula) trees respond to severe (50—100%) manual defoliation by delayed inducible resistance (DIR). This plant response to defoliation is characterized by a decline in the nutritional quality of leaves for immature insects for several years after defoliation events, and concomitant changes in leaf chemistry that may be detrimental to insect nutrition, that is, a decline in leaf nitrogen and an increase in leaf phenols. Two explanations of delayed inducible resistance have been proposed. (1) The active defense response hypothesis claims that delayed inducible resistance is an active response to defoliation per se rather than merely a passive consequence of recovery from the stress of severe defoliation. (2) In contrast, the carbon—nutrient balance (CNB) hypothesis claims that delayed inducible resistance is caused by nutritional stress resulting from severe defoliation. We used two experiments to test these hypotheses. (1) In a three—way factorial field experiment we reared spear—marked black moth (Rheumaptera hastata) larvae on Alaska paper birch (B. resinifera) saplings that had experienced combinations of 100% manual defoliation and fertilization with N and P in previous years, and measured larval survival and pupal mass. In association with these measurements of larval performance, we assayed leaf condensed tannin levels and the concentrations of N and P in leaves, and correlated the results of these assays with larval performance. (2) In a laboratory experiment we tested the biological activity of condensed tannin and linalool, the major secondary metabolites of Alaska paper birch leaves, by treating leaves collected from previously undefoliated Alaska paper birch saplings with combinations of condensed tannin and linalool, and measuring the performance of spear—marked black moth larvae reared on these leaves. Our results supported predictions of the carbon—nutrient balance hypothesis. We found that fertilization with nitrogen, the nutrient limiting growth of Alaska paper birch in our study site, mitigated delayed inducible resistance, and that condensed tannin is likely to be the major chemical cause of delayed inducible resistance in Alaska paper birch. In our field experiment we also found that fertilization of Alaska paper birch with phosphorus, a nutrient that does not limit the growth of Alaska paper birch in our study site, affected levels of condensed tannin in leaves and the sapling's defoliation history influenced this effect. Thus, future studies of the effects of mineral nutrition on secondary metabolite production by woody plants and their responses to herbivory should consider nutrients that do not limit growth in addition to those that do limit growth.

Plant nutrient supply determines competition between phytophagous insects

“…Bryant et al [13] found that complete artificial defoliation of birch (Betula resinifera) increased tannin concentrations in plants in a low-nutrient treatment, but had no effect on those under high nutrients. Previous damage by gypsy moth populations increased phenolic concentration in unfertilized Quercus pinus foliage, but not in fertilized trees [40].…”

Influence of tree growth rate, shoot size and foliar chemistry on the abundance and performance of a galling adelgid

“…Studies examining the relationship between insect performance and plant chemistry have also reported varying results (Tija & Houston 1975;Zucker 1982;Waring & Price 1990;Hartley & Lawton 1992;Waring & Cobb 1992;Bryant et al 1993;Hartley & Jones 1997). Nevertheless, these studies generally found a positive relationship between insect performance and plant nitrogen content, and a negative relationship to secondary compounds (e.g.…”

Mechanisms of plant defense against insect herbivores

“…reduced the pupal mass and survival of Rheumaptera hastata (L.) larvae. 52 It has been reported that induction of tannins in Populus tremuloides Michx. leaves in response to wound-and herbivore occurs by transcriptional activation of the flavonoid pathway.…”