Bl. Waite et Rw. Hutkins, BACTERIOCINS INHIBIT GLUCOSE PEP-PTS ACTIVITY IN LISTERIA-MONOCYTOGENES BY INDUCED EFFLUX OF INTRACELLULAR METABOLITES, Journal of applied microbiology, 85(2), 1998, pp. 287-292
Glucose transport by the phosphoenolpyruvate (PEP)-dependent phosphotr
ansferase system (PTS) of Listeria monocytogenes is inhibited by the b
acteriocins nisin, pediocin JD and leuconocin S. To investigate the me
chanism of inhibition, PTS activity assays were performed with permeab
ilized, bacteriocin-treated L. monocytogenes Scott. A cells. In the pr
esence of exogenous PEP, nisin stimulated the PTS while both pediocin
JD and leuconocin S partially inhibited its activity. These results su
ggested that PTS enzymes were still active in bacteriocin-treated cell
s and that bacteriocin-induced PEP efflux may be a mechanism for inhib
ition of the PTS. To verify that PEP did efflux from bacteriocin-treat
ed L. monocytogenes Scott A cells, intracellular and extracellular PEP
were measured by HPLC. All three bacteriocins induced efflux of PEP.
Nisin, pediocin ID and leuconocin S also induced efflux of AMP, ADP an
d ATP. These studies indicate that bacteriocin inhibition of the gluco
se PEP:PTS in L. monocytogenes is due to efflux of intracellular metab
olites, particularly PEP.