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Even cherry seed collected from the soil under a galled tree can be contaminated and infect the subsequent seedlings (Tourney, 1900). Regardless of the source of the planting stock, the planting site must be considered. Seedlings from the same nursery source planted at two locations in Oregon and two in New York State showed a 70% incidence of galling at one of the Oregon production site versus 3% at the other Oregon site and 12 and 6% at the New York sites (Moore, 1976). Similarly, when symptomless cherry seedlings from one production site were lined out besides those from another site, one lot was severely galled at harvest but not the other (Young, 1954).

Another mechanism for agrocin-84 activity was proposed by Smith and Hindley (1978) who found that incubation of the pathogenic strain C58 in the 36 L. W. MOORE AND D. A. COOKSEY presence of agrocin 84 reduced its ability to bind to host cells. It was proposed that agrocin 84 inhibited tumor induction by causing a disruption of the cell envelope structure required for binding to the host. However, biological control in the field is not always correlated with the production of agrocin 84. Three reports (Schroth and Möller, 1976; Moore, 1977; Cooksey and Moore, 1980) have shown that some agrocin 84-resistant A.

Acad. Sei. A. 44, 344-349. Braun, A. C. (1959). Proc. Natl. Acad. Sei. A. 45, 932-938. Braun, A. C , and Mandle, R. J. (1948). Growth 12, 255-269. Braun, A. C , and Wood, H. N. (1976). Proc. Natl. Acad. Sei. A. 73, 496-500. Brown, J. , and Evans, M. M. (1933). Phytopathology 23, 97-101. Brown, N. A. (1929). J. Agric. Res. 39, 747-766. Chamberlain, G. C. (1962). Can. Plant Dis. Surv. 42, 208-211. Chilton, M. , Drummond, M. , Merlo, D. , Montoya, A. , Gordon, M. , and Nester, E. W. (1977). Cell 11, 263-271.

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