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. 2006 Nov 10;189(4):1189–1198. doi: 10.1128/JB.01254-06

FIG. 2.

FIG. 2.

Model of the mechanisms behind killing (A) and immunity (B) of classIIa bacteriocins. (A) The bacteriocin (red) employs man-PTS (orange) as a target receptor upon approaching susceptible cells (1). It binds to the components IIC (C) and IID (D) of mannose-PTS (2) and somehow causes leakage of solutes across the cytoplasmic membrane (3) and eventually cell death. (B) In immune and non-bacteriocin-producing cells (1), the immunity protein (pink) is nonassociated or loosely associated with the receptor proteins. When bacteriocin is exogenously added or produced by the bacteria themselves (2), the immunity protein is tightly associated with the receptor to prevent the bound bacteriocin on the receptor from forming lethal pores in the cytoplasmic membrane (3). In all cases, the cytoplasmic component IIAB (AB) is in contact with its membrane-located partners, but without being directly involved in a receptor function or in an immunity function. CW, cell wall; CM, cytoplasmic membrane. The model is based on published work (41, 47, 103) and unpublished work (Diep and Holo, unpublished).