Creation and Complementation of Pathogenicity Mutants of Erwinia amylovora. Eva M. Steinberger. Department of Plant Pathology, Cornell University, Ithaca, NY 14853, U.S.A.. Steven V. Beer. Department of Plant Pathology, Cornell University, Ithaca, NY 14853, U.S.A.. MPMI 1:135-144. Accepted 15 April 1988. Copyright 1988 The American Phytopathological Society.

The transposon Tn5 was used to create mutants of Erwinia amylovora, altered in their pathogenic capabilities on immature pear fruits or apple seedlings. Five mutant classes were established based on the following phenotypes: loss of pathogenicity, reduction in virulence, loss of the ability to cause the hypersensitive reaction (HR) in tobacco, reduction in the ability to cause the HR, and diminished production of extracellular polysaccharide (EPS). The genes responsible for these phenotypes were shown to be chromosomally inherited. A decrease in EPS production was correlated with low virulence, indicating that EPS acts as a virulence factor in E. amylovora, rather than as a pathogenicity factor. From two overlapping cosmid clones, a gene cluster of at least five genes was identified by genetic complementation. The cluster includes genes involved in the compatible interaction with a host and genes encoding the induction of the HR in a nonhost. This work provides evidence that genes encoding pathogenicity and hypersensitivity determinants are closely linked and that those involved in hypersensitivity are also required for pathogenicity.