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In vivo cluster formation of nisin and lipid II is correlated with membrane depolarization.

ABSTRACT: Nisin and related lantibiotics kill bacteria by pore formation or by sequestering lipid II. Some lantibiotics sequester lipid II into clusters, which were suggested to kill cells through delocalized peptidoglycan synthesis. Here, we show that cluster formation is always concomitant with (i) membrane pore formation and (ii) membrane depolarization. Nisin variants that cluster lipid II kill L-form bacteria with similar efficiency, suggesting that delocalization of peptidoglycan synthesis is not the primary killing mechanism of these lantibiotics.

SUBMITTER: Tol MB

PROVIDER: S-EPMC4432147 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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In vivo cluster formation of nisin and lipid II is correlated with membrane depolarization.

Tol Menno B MB Morales Angeles Danae D Scheffers Dirk-Jan DJ

Antimicrobial agents and chemotherapy 20150413 6

Nisin and related lantibiotics kill bacteria by pore formation or by sequestering lipid II. Some lantibiotics sequester lipid II into clusters, which were suggested to kill cells through delocalized peptidoglycan synthesis. Here, we show that cluster formation is always concomitant with (i) membrane pore formation and (ii) membrane depolarization. Nisin variants that cluster lipid II kill L-form bacteria with similar efficiency, suggesting that delocalization of peptidoglycan synthesis is not th ...[more]

PMID: 25870072

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