'Cavity disease', defined as the rapid degradation of the sporocarps of white button mushrooms, is caused by Burkholderia gladioli pv. agaricicola, a member of Pseudomonaceae. The specific strain analysed in this thesis, BG 164, was isolated from New Zealand, but the disease has also been sporadically reported in Europe.
Nine mutants that did not cause cavity symptoms ('no-cavity') were isolated by transposon mutagenesis of the BG 164 derivative, BG 164R. Eight mutants had altered flagella number, did not secrete protease, had a highly reduced capacity to secrete chitinase and did not degrade mushroom mycelia. All these eight mutations were clustered in the GSP (General Secretory Pathway) operon. A cosmid, carrying 23.4kb genomic DNA, pCosGSP, complemented all mutations, which along with mapping of the cosmid, confirms that the cosmid has most or all of the functional gsp operon.
The ninth mutant, BGII-107, secreted protease, although it did not form cavity on mushrooms. The DNA sequence analysis suggests that the mutation is in a polyketide synthetase gene. Interestingly, the mutant can also be complemented by the gsp operon-containing cosmid, suggesting the presence of a polyketide synthetase gene adjacent to the GSP genes.
Cavity disease initiation, in contrast to most of the other diseases, requires a very high inoculum of the pathogen, suggesting a probable reason for the sporadic appearance of the disease. Studies on the indigenous non-pathogenic bacterial population of mushrooms led to the identification of a natural antagonist of BGI64R, Ewingella americana (PRC120), in the sporocarp tissue. Population studies indicated the involvement of polymicrobial interactions and a quorum sensitivity-dependent induction of Cavity disease expression
