ECBI AND ECBR - HOMOLOGS OF LUXI AND LUXR AFFECTING ANTIBIOTIC AND EXOENZYME PRODUCTION BY ERWINIA-CAROTOVORA SUBSP BETAVASCULORUM

Erwinia carotovora subsp. betavasculorum Ecb168 causes vascular necros is and root rot of sugar beet and produces an antibiotic(s) that is an tagonistic against other Erwinia spp. EcbI(-) mutants of Ecb168, each containing a single transposon insertion in the ecbI gene (for Erwinia carotovora subsp. betavasculorum inducer), do not produce detectable levels of extracellular protease or antibiotic(s), and express less pe ctate lyase activity and virulence than the wild-type strain. A plasmi d containing the cloned ecbI gene complemented the EcbI(-) mutants for these phenotypes. Protease production by EcbI(-) mutants grown on aga r surfaces was restored by neighboring cells of Escherichia coli conta ining ecbI. Production of a diffusible N-acylhomoserine lactone autoin ducer by wild-type Ecb168 was detected with indicator strains of E, co li and Agrobacterium tumefaciens. EcbI(-) mutant strains did not produ ce an autoinducer detected by the indicator strains. Antibiotic produc tion by EcbI(-) mutants was restored by cell-free culture supernatants of Ecb168 or E. coli containing a cloned ecbI gene. The predicted ami no acid sequence of EcbI is similar to those of Carl, ExpI, and HsII, three LuxI homologs required for production of a diffusible N-acylhomo serine lactone autoinducer in Erwinia carotovora subsp. carotovora. A luxR homolog, termed ecbR (for Erwinia carotovora subsp. betavasculoru m regulator), is convergently transcribed and overlaps with ecbI by 17 bp at their 3' ends. These results are consistent with the hypothesis that a quorum-sensing system related to the prototypic luxl-luxR gene pair controls antibiotic and exoenzyme production in Erwinia carotovo ra subsp. betavasculorum.