Gene for pathogenicity and ability to cause the hypersensitive reaction cloned from Erwinia amylovora

Localization of transposon insertions in pathogenicity mutants of Erwinia amylovora and their biochemical characterization

“…A similar phenomenon was described for complementation in planta of the spontaneous mutants P66 and 4S2 (Bennett, 1980). E. amylovora strain P66 has a defect for induction of HR on non-host plants (Walters et al, 1990), whereas strain 4S2 is deficient in EPS synthesis. By reisolation of the unchanged mutants from ooze on pear tissue we conclude that no exchange of DNA occurred among the E. amylovora mutants in planta, in contrast to the DNA uptake observed in cultures of Haemophilus influenzae or Neisseria gonorrhoeae (Goodman & Scocca, 1988).…”

“…In search of virulence mechanisms for the fire blight pathogen E. arnylovora, deficiencies in EPS synthesis and loss of its ability to induce HR on non-host plants (Steinberger & Beer, 1988;Barny et al, 1990;Walters et al, 1990;Bellemann et al, 1990) were found to be correlated with a loss of pathogenicity. We report here the genetic characterization of Tn5 mutants of E. arnylovora and the effect of the mutations on bacterial EPS synthesis.…”

The virulence of Erwinia amylovora: molecular genetic perspectives

“…This indicates that genes encoding factors essential for the pathogenicity of E. arnylovora are expressed in E. coli. However, E. coli harbouring cosmid clones carrying only part of this region fail to induce a HR (Walters et al, 1990;Barny et al, 1990). Perhaps more surprising was the observation that certain transposon insertions in pCPP430, which abolish HR when reintroduced onto the chromosome of E. arnylovora, could be complemented by E. coli .…”

“…The first such mutant studied in any detail was the spontaneous mutant P66 identified by Billing (Bennet & Billing, 1978 ;Bennet, 1980). This mutant was not only avirulent but also failed to elicit a necrotic hypersensitive response (HR) when inoculated into a non-susceptible host such as bean or tobacco (Walters et al, 1990). Recently, transposon insertion mutants with the same phenotype as P66 have been isolated (Steinberger & Beer, 1988;Barny et al, 1990).…”

“…Recently, transposon insertion mutants with the same phenotype as P66 have been isolated (Steinberger & Beer, 1988;Barny et al, 1990). These insertions were localized to a single region of approximately 40 kb of the E. amylocora chromosome and cosmid clones capable of complementing these insertions and mutant P66 have been isolated by a number of groups (Steinberger & Beer, 1988;Barny et al, 1990;Walters et al, 1990). This large virulence region has been further subdivided, as described below.…”