2.4.12
INVOLVEMENT OF THE SEXUAL CYCLE OF MYCOSPHAERELLA GRAMINICOLA IN DISEASE DEVELOPMENT IN WINTER WHEAT?

T HUNTER, RR COKER, DJ LOVELL and DJ ROYLE

IACR-Long Ashton Research Station, University of Bristol, Long Ashton, Bristol BS1 8 9AF, UK

Background and objectives
Leaf blotch of wheat, caused by Mycosphaerella graminicola (Fuckel) Schroeter, (anamorph Septoria tritici Rob. Ex Desm.), is a disease of global importance. In winter wheat it often causes severe crop damage, especially during summer, attributable to repeated cycles of the asexual stage of the pathogen. In the UK, ascospores of the sexual stage are responsible for initiating most of the early infection of winter wheat crops during the autumn [1]. However, subsequent infection of the upper crop leaves has been attributed entirely to splash dispersal of pycnidiospores from infected basal tissue during heavy rains. More recent work, however, has shown that inoculum is not confined to the base of the crop and that transfer of inoculum can occur under less rigorous wetness conditions, being influenced by the position of developing leaves in relation to infected leaf layers [2]. Another possible means of disease spread within a crop during summer is by airborne ascospores, which may play a more important role than was previously recognized. This work describes methods and observations on the identification and occurrence of the sexual stage in winter wheat crops, with the object of obtaining a better understanding of its role in the epidemiology of the disease during the main period of crop growth.

Materials and methods
Airborne ascospores of M. ;graminicola were trapped using Burkard suction traps in field sites over a number of years. Spores were authenticated by transferring the trap tapes after exposure onto agar media to allow development of the distinctive germination pattern of budding conidia. Development of ascocarps was monitored at monthly intervals on naturally senescent wheat, cv. Riband, and also in field trials within the growing crop on unsprayed plants from April (GS 32) to July (GS 85). Inoculations were of pot-grown winter wheat, using isolates of S. ;tritici (derived from single-ascospore cultures), to determine the temporal development of the sexual stage.

Results and conclusions
Spore catches in the early 1990s indicated that the major periods of ascospore release occurred during October to December, with a secondary peak in June/July. However, recent trappings (1995-97) have shown a consistent trend for ascospores to be present throughout the year, with increasing numbers detected during summer months when the crop is actively growing. Production of spores from ascocarps (sexual fruiting bodies) on senescent material from the previous year's unharvested wheat crops was mainly completed by mid-winter; thus, spores caught during the summer months must have arisen from fresh ascocarps. Natural development of the sexual stage was found in the developing crop early in April (GS 32) on leaf layer 8 and was probably present before this date on earlier leaves. Thereafter, there was progressive development of maturing ascocarps on successive leaf layers, culminating in their being found on flag leaves by mid-July (GS 85-87). These observations indicate that the sexual stage develops throughout the growth of winter wheat crops in the UK, which emphasizes their possible contribution to large genetic variation within populations. The ability of the pathogen to respond to selection pressures, either chemical or environmental, is enhanced by the possibility of continued genetic exchange throughout the season. Preliminary inoculation experiments have shown that ascospores are capable of causing disease under conditions similar to those necessary for the development of pycnidiospore infections. The relative contribution of the sexual stage to the final disease severity within a crop is unknown. However, in conditions when pycnidiospore inoculum is low, or conditions for transfer are limiting, the presence of the sexual stage within the growing season may have a major bearing on final severity levels.

References
1. Shaw MW, Royle DJ, 1989. Plant Pathology 38, 35-43.
2. Lovell DJ, Parker SR, Hunter T, Royle DJ, Coker RR, 1997. Plant Pathology 46, 126-138.