SUMMARY: A transposon insertion mutant with defective release of several exoenzymes has been characterized. The Tn insertion mutation was located in the previously described locus at 0 min on the chromosomal map and caused several exoenzymes to remain in cell-bound form. At least one of the exoenzymes, elastase, was accumulated in the periplasmic space. The periplasmic elastase had the same as the extracellular enzyme produced by the wild-type strain. The virulence of the mutant was comparable to that of wild-type strains in experimental burn infection in mice. The presence of an easily selectable antibiotic resistance marker in the locus offers the possibility of cloning the gene(s) involved in exoprotein secretion.


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