A function of DivIVA in Listeria monocytogenes division site selection

The cell division protein DivIVA influences protein transport via the accessory SecA2 secretion route in Listeria monocytogenes. In contrast, DivIVA from the closely related bacterium Bacillus subtilis contributes to division site selection via the MinCDJ system. However, no classical min phenotype, i.e. filamentation and minicell production was observed with a listerial ΔdivIVA mutant. This has prompted the speculation that division site selection is DivIVA-independent in L. monocytogenes. We addressed this question with genetic, cytological and bacterial two-hybrid experiments and the data obtained correct this view. DivIVA not only binds to MinJ but also directly interacts with MinD. Experiments with fluorescently tagged proteins showed that localization of MinC and MinD was clearly DivIVA-dependent, whereas localization of MinJ was not. An impact of DivIVA on cell division was confirmed by careful comparisons of cell size distributions of divIVA and secA2 mutants. Gene deletion studies and epistasis experiments consistently reinforced these findings, and also revealed that MinJ must have a DivIVA-independent function. The frequency of minicell formation is low in L. monocytogenes min mutants. However, since listerial minicells might be useful as carriers for the introduction of therapeutic compounds into eukaryotic cells, we present a strategy how minicell frequency can be increased.