Abstract

A nonpathogenic Erwinia amylovora transposon mutant that has an insertion in the guaB gene was isolated. The mutation results in a nutritional requirement for guanine or xanthine, and loss of ability to produce ooze on immature pear fruit and to cause symptoms in the apple seedling assay. The mutant expressed other known virulence determinants including extracellular polysaccharide and had an intact hrp/dsp cluster. In addition it was able to grow in host tissue, although the population size in planta was maintained at a considerably lower level than that seen with the parent strain. The inability of the Erwinia amylovora guaB mutant to cause disease indicates that levels of guanine in plant tissue are likely to be insufficient to maintain optimal growth via the purine salvage pathway. This, in turn, appears to compromise the ability of the mutant to develop a sufficiently large population size in planta to overcome host defence mechanisms and cause disease symptoms. This indicates that a functional de novo guanine synthetic pathway is important for Erwinia amylovora to grow on plant tissue and cause disease.

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