IACR-Long Ashton Research Station, University of Bristol, Long Ashton, Bristol BS18 9AF, UK

Background and objectives
Leaf blotch (Septoria tritici) is the most serious foliar fungal disease of winter wheat in western Europe. Considerable yield loss can be caused if it becomes severe on the flag and second leaves. In years of severe disease, generalized crop loss models estimate losses in the UK to be >20 ;million. Inoculum of S. ;tritici, occurring within the basal leaves of winter wheat crops, is spread to the top of the canopy by rainfall splash. This mechanism is commonly accepted to be a key limit to disease progression. A convincing association has been shown to occur between the number of wet days in May (the stem extension period for most UK wheat crops) and disease severity at growth stage (GS) 72. A relationship between S.  ;tritici severity and final plant height has been reported [1]. This has been attributed to a possible linkage, or pleiotropy, of the genes controlling both height and resistance. However, recent studies suggested that factors of crop growth and canopy structure, such as rates of stem elongation and leaf emergence, might profoundly affect the risk of inoculum transfer onto the upper leaves, thereby constituting disease escape[2]. This study aims to identify the importance of such factors in determining disease risk and their contribution to the expression of overall field resistance.

Materials and methods
Twice-weekly measures of crop structure and inoculum position, were obtained on a wide range of cultivars that were variously susceptible to S.  ;tritici and in which canopy structure differed. These measures were also done on two cultivars, Riband and Cadenza, in which plant height was reduced by application of plant growth regulator, or in which inoculum amount and location were affected by application of fungicide just prior to stem extension. The risk of disease progression was estimated by a measure of 'lesion proximity' (location of inoculum, relative to the emerging leaf) [3], and assessments of disease severity were made at weekly intervals.

Results and conclusions
During stem extension, emerging leaves often grew away from sources of inoculum, thus reducing lesion proximity. This occurred most profoundly in seasons in which rainfall was limiting and in cultivars which exhibited rapid stem extension. The mean lesion proximity (GS 33-39) for 29 cultivars was found to be significantly correlated with the rate of stem extension (R2=0.77). Therefore, the risk of inoculum transfer to the upper canopy leaves was generally less in crops that had rapid rates of stem extension. However, only poor correlations were obtained between lesion proximity and final disease severity for these cultivars. This can partly be explained by the varying degrees of intrinsic susceptibility between the cultivars studied. However, in experiments in which PGR was used to alter plant height, intrinsic susceptibility remained constant for a given cultivar. In these experiments, plant height was reduced when PGR had been applied, although there was no effect on lesion height. Consequently, lesion proximity and, therefore, risk of inoculum transfer was increased and resulted in an increase in final disease severity on the upper leaves. In experiments in which fungicide was used, plant height and intrinsic susceptibility remained constant but lesion proximity was reduced, resulting in significantly less final disease severity on the upper leaves. These studies confirm the existence of disease escape mechanisms and show that the rate of stem extension is a major contributory trait. Although a particular cultivar may possess the traits required to escape disease, its expression is dependent upon environmental interactions. Therefore, for a given cultivar, escape will occur to varying degrees across sites and seasons. Disease escape plays a major role in expression of field resistance and, therefore, the inclusion of such traits within future breeding programmes should contribute to durable resistance to S. ;tritici.

1. Tavelia CM, 1978. Euphytica 27, 577-80.
2. Lovell DJ, Parker SR, Hunter T, Royle DJ, Coker RR, 1997. Plant Pathology 47, 126-38.
3. Lovell DJ, Parker SR, Hunter T, Royle DJ, Flind AC, 1997. Aspects of Applied Biology 48, 151-54.