Ascospores as primary inoculum for epidemics of white leaf spot (Mycosphaerella capsellae) in winter oilseed rape in the UK

In the UK, conidia of Pseudocercosporella capsellae, the anamorph of Mycosp haerella capsellae, were observed on white leaf spot lesions on leaves thro ughout the growing season. Ascomata were not observed on lesions on either green or senescent leaves, although stromatic knots and spermogonia were oc casionally seen in summer. However, spermogonia and protoascomata were prod uced in white leaf spot pod and stem lesions in early summer. Protoascomata continued to mature after harvest in these lesions on the debris. Mature a scomata subsequently developed by early autumn, but were exhausted by early January and did not overwinter. A diurnal periodicity in numbers of air-bo rne M. capesellae ascospores discharged from infected debris was observed w ith a Burkard spore sampler, with greatest numbers of ascospores collected near the middle of the day; the records also suggested that ascospores were released in response to wetting by dew or rain. Studies of natural white l eaf spot epidemics in winter oilseed rape provided evidence that air-borne ascospores are the primary inoculum for initiating epidemics in the autumn in the UK. White leaf spot disease gradients over 100 m across a winter oil seed rape crop at Rothamsted were fitted by both negative exponential and i nverse power-law models, with gradient slopes suggesting the deposition of air-borne spores dispersed from a single local source of inoculum. In compa rison, no obvious white leaf spot gradients were observed over 250 m in a s everely diseased crop near North Petherton, Somerset, suggesting that the a ir-borne spores were dispersed from a number of more distant sources in the area. Both patterns of disease were unlikely to have been initiated by P. capsellae conidia, which are dispersed only very short distances by rain-sp lash. However, once epidemics have been initiated by air-borne ascospores i n the autumn, subsequent disease spread within an infected crop is dependen t only on splash-dispersed conidia. A revised disease cycle of the pathogen is proposed.