1887

Abstract

It has been suggested that resistance to class IIa bacteriocins occurs at either a low or a high level. In listerial strains, low-level resistance (2–4-fold) to class IIa bacteriocins is attributed to alterations in membrane lipid composition. In and , high-level resistance (1000-fold) correlates with inactivation of the operon, which encodes the EII mannose permease of the phosphotransferase system (PTS). Previous studies reported that in , high-level resistance involved the factor and the ManR activator. In this investigation, three genes associated with the resistance of JH2-2 to divercin V41, a pediocin-like bacteriocin from V41, were clearly identified by screening an insertional mutant library of JH2-2. These genes correspond to the well-known gene, which encodes factor, and to genes encoding a glycerophosphoryl diester phosphodiesterase (GlpQ) and a protein with a putative phosphodiesterase function (PDE). Resistance of the three mutants defective in the aforementioned genes appeared to be graduated: the mutant was more resistant than the mutant, which was more resistant than the mutant. Moreover, this resistance was specific to class IIa bacteriocins.

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2007-05-01
2020-04-10
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