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1 UMR-INRA 1014 SECALIM, ENITIAA, Rue de la Géraudière, BP 82225, Nantes Cedex 3, France
2 Laboratoire de Microbiologie de l'Environnement, EA 956, USC INRA 2017, IRBA, Université de Caen, Caen Cedex, France
Correspondence
Djamel Drider
drider{at}enitiaa-nantes.fr
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 (24-fold) to class IIa bacteriocins is attributed to alterations in membrane lipid composition. In Listeria monocytogenes and Enterococcus faecalis, high-level resistance (1000-fold) correlates with inactivation of the mptACD operon, which encodes the EIIMant mannose permease of the phosphotransferase system (PTS). Previous studies reported that in L. monocytogenes, high-level resistance involved the
54 factor and the ManR activator. In this investigation, three genes associated with the resistance of Ent. faecalis JH2-2 to divercin V41, a pediocin-like bacteriocin from Carnobacterium divergens V41, were clearly identified by screening an insertional mutant library of Ent. faecalis JH2-2. These genes correspond to the well-known rpoN gene, which encodes
54 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 rpoN mutant was more resistant than the glpQ mutant, which was more resistant than the pde mutant. Moreover, this resistance was specific to class IIa bacteriocins.
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