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Applied and Environmental Microbiology, August 2004, p. 4486-4490, Vol. 70, No. 8
0099-2240/04/$08.00+0 DOI: 10.1128/AEM.70.8.4486-4490.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Plant Pathology, National Institute for Plant Protection, Chem-Tuliem, Hanoi, Vietnam,1 Department of Horticulture and Life Sciences, Cheju National University,3 Jeju Hi-Tech Industry Development Institute,4 Department of Biochemistry, Cheju National University Medical School, Jeju, Republic of Korea2
Received 24 December 2003/ Accepted 6 April 2004
The ability of glycinecin A, a bacteriocin derived from Xanthomonas campestris pv. glycines 8ra, to kill closely related bacteria has been demonstrated previously by our group (S. G. Heu et al., Appl. Environ. Microbiol. 67:4105-4110, 2001). In the present study, we aimed at determining the glycinecin A-induced cause of death. Treatment with glycinecin A caused slow dissipation of membrane potential and rapid depletion of the pH gradient. Glycinecin A treatment also induced leakage of potassium ions from X. campestris pv. vesicatoria YK93-4 cells and killed sensitive bacterial cells in a dose-dependent manner. Sensitive cells were killed within 2 h of incubation, most likely due to the potassium ion efflux caused by glycinecin A. These results suggest that the bactericidal mechanism of action of glycinecin A is correlated with the permeability of membranes to hydroxyl and potassium ions, leading to the lethal activity of the bacteriocin on the target bacteria.
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