The effect of long-term N-supply on growth, scab resistance and phenolic compounds in the leaves of two apple cultivars was studied. The different pools of phenylpropanoids (hydroxycinnamic acids, dihydrochalcones) and flavonoids (flavonols, catechins, procyanidins) were quanitfied by HPLC from non-infected and inoculated leaves representing different ontogenetic stages. Scab incidence was also evaluated. Strictly following the carbon-nutrient-balance hypothesis, apple trees responded to high N-supply with increased shoot growth and with a reduced accumulation of total phenolic compounds in their leaves. This was shown for the cultivar 'Golden Delicious', which is susceptible to the scab disease caused by Venturia inaequalis, and for the resistant cultivar 'Rewena'. Whereas high N-fertilization increased the susceptibility of 'Golden Delicious', it did not decrease the resistance of 'Rewena' despite of the pronounced reduction of phenolic concentrations. Thus, a simple C trade off between growth-related metabolism and secondary metabolism cannot solely explain changes in defensive potential.

The paper shows that N‐induced vigorous shoot growth increases susceptibility of apple trees to Venturia inaequalis. This is due to a weakened defence in infected leaves of the high N cultures showing large lesions with excessive sporulation, whereas infected leaves from the low N cultures exhibited successful defence with only small chlorotic lesions and no sporulation. This might be explained by biosynthesis of phenylpropanoids in the young leaves of the resistant trees. A negative correlation between shoot growth of apple trees and the concentration of phenolic compounds in young leaves was found. Studies on in vitro shoot cultures revealed that the availability of sugars for the phenylpropanoid pathway is a strong regulatory factor. The ratio of sucrose and nitrogen in the medium influenced the total level of secondary products in the in vitro grown plantlets. Moreover, the relative deficiency of sugars was responsible for a metabolic block mainly at the level of glucosyl transferase and concomitant aglycone accumulation.

The allocation of plant internal resources to growth processes (primary metabolism) and to defensive compounds (secondary metabolism) is determined by plant internal competition for common substrates and energy. In order to contribute to the discussion about environmental impacts on this trade-off between demands for growth and defence, we extended a complex plant growth model to simulate the formation of defensive compounds on the whole plant level, depending on the dynamics of the environmental conditions light, nutrients and water. In this paper, we present and apply the model to simulate the effects of different N fertilizer applications on growth and resistance of young apple trees (cv "Golden Delicious"). The results show that model predictions are able to describe the observed relation between growth rate and phenylpropanoid concentrations in young leaves of apple trees, and can assist in the interpretation of experimental findings. Finally, we estimate costs and benefits of investment into defence in a scenario, in which an attack by the leaf pathogen Venturia inaequalis is simulated.

Apple scab, one of the most damaging diseases in apple worldwide is caused by the fungal pathogen Venturia inaequalis. Pathogen-induced gene expression was analyzed in leaves of greenhouse-and field-grown trees of the scab susceptible cultivar Golden Delicious and the resistant cultivar Rewena using the macroarray technique. The results show that the defence of the Vf-resistant cultivar Rewena is based on different mechanisms than the basal defence response of the susceptible Golden Delicious: whereas lignification seems to play an essential role in scab defence of Rewena, a thaumatin-like as well as a flavonoid gene are assumed to be involved in the mostly insufficient defensive response of Golden Delicious. Furthermore, a method was developed for quantification of the V. inaequalis in infected leaves using real-time quantitative reverse transcription-PCR.