Abstract
Nisin resistance in Listeria monocytogenes ATCC 700302 is a complex phenotype involving alterations in both the cytoplasmic membrane and the cell wall and a requirement for divalent cations. In addition to a lower ratio of C15 to C17 fatty acids than in the wild-type strain (A. S. Mazzotta and T.J. Montville, J. Appl. Microbiol. 82: 32-38, 1997), this nisin-resistant (Nisr) strain contained significantly more zwitterionic phosphatidylethanolamine and less anionic phosphatidylglycerol and cardiolipin. The extraction of cardiolipin was enhanced by a penicillin-lysozyme step to disrupt the cell wall. This study is the first to quantify the phosphatidylethanolamine component of the L. monocytogenes cytoplasmic membrane. While these cytoplasmic membrane changes were induced by nisin, the Nisr strain also showed altered sensitivities to cell wall-acting compounds, even when grown in the absence of nisin, suggesting a constitutive alteration in the strain's cell wall. A model which integrates the roles of the cell membrane, cell wall, and divalent cations is presented. Finally, nisin resistance in L. monocytogenes ATCC 700302 conferred cross-resistance to the class IIa bacteriocin pediocin PA-1 and the class IV leuconocin S.
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