Three nurseries produced apple rootstocks (M9) and budwood (cv. Royal Gala), which they exchanged at the end of the first year. Each nursery then budded its own budwood onto the rootstocks it had produced and that from the other two nurseries. Budded trees were grown on for a further year before being planted at HRI, East Malling in southern England; NIHPBS, Loughgall in Northern Ireland; and ADAS, Rosemaund in the West Midlands of England. Canker development was monitored twice a year. The position of the infected trees within the orchard was recorded, as was the position of the canker on each tree (main-stem or peripheral). Nectria galligena was isolated from representative cankers and analysed using molecular techniques. At the sites in Northern Ireland and HRI there was a strong positional effect, especially of peripheral cankers, indicating that most of the inoculum was external and had been spread from neighbouring orchards. There was little or no positional effect on main-stem cankers at any of the three sites. The proportions of different isolates taken from peripheral cankers was different in Northern Ireland from that in England, suggesting different populations associated with the geographic areas. In contrast, the populations of N. galligena obtained from main-stem cankers were very similar in England and Northern Ireland. It was concluded that a small proportion of trees developing canker were infected during propagation, with no symptom development until after planting. In a second trial it was demonstrated that trees infected during the propagation phase, and particularly at budding and heading back, could develop canker up to 3 years later. While it is clear that some canker developing in the orchard can be associated with the nursery of production, in climatic conditions conducive to the formation and dissemination of conidia, inoculum from surrounding infected orchards is the primary source of the pathogen. Aerial spread is therefore an essential element of the epidemiology of N. galligena , and its control is a crucial part of any canker-control programme.

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S U M M A R YI n laboratory experiments germinating conidia penetrated lenticels and wounds but not the intact surfaces of apples. Date of harvest had no significant effect on the numbers of apples infected with Nectria galligena but the earliest picks rotted first in barn store. Inoculations of unpicked apples resulted in small arrested lesions which only developed into progressive rots after a considerable period in store. Rots developed most quickly from inoculations made between mid-August and mid-September. The size of rot increased with spore number and many inoculations with 10-100 conidia remained as arrested lesions.Arrested lesions developed 10-1 5 days after unripe apples were inoculated and consisted of a zone of fungal colonization surrounded by suberized, necrotic cells in which compounds toxic to both N . galligena and Penicillium expansum were detected. No antifungal compounds were found in progressive rots of mature apples or in healthy apples of any age. Antifungal activity, measured by inhibition of P. expansum, was greatest 15-20 days from inoculation of unripe apples with N . galligena but decreased after a total of 35 days incubation at 20 "C. Much less antifungal activity was produced in ripe or dessert apples.

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S U M M A R YTrapping of ascospores and conidia of Nectria galligena Bres. released from cankers on Bramley's Seedling apple trees over a period of three years showed that ascospores were most prevalent in the spring and early summer, and conidia from early summer to late autumn. Few ascospores were released in late summer or mid-winter but a minor period of discharge occurred in autumn.The distribution of cankers within trees in various orchards was also examined, and most were found to occur at the junctions of different seasons' growth. Possible reasons for this are discussed.