8 μm, and no minicells were observed. These data indicate that overexpression of MinEEc is not able to elongate B. subtilis cells or to produce a minicell phenotype. Deletion of B. subtilis min genes causes minicell formation and slight cell elongation (Levin et al., 1992, 1998). The possibility that proteins of the E.

coli Min system can restore the defects caused by a lack of their homologues in B. subtilis was investigated. The experiments were carried out without xylose induction and using two different xylose concentrations (0.05% and 0.3% w/v). The control experiments selleck kinase inhibitor with the parental strains IB1141 (ΔminCBs) and IB1056 (ΔminDBs) were performed without and in the presence of 0.05% xylose. In comparison with the wild-type cells (MO1099), with average cell lengths 2.3 μm, the ΔminCBs (IB1141) cells were elongated, with average cell lengths 3.3 μm without xylose (Fig. 2a) and 3.1 μm with 0.05% xylose (not shown). The minicells represented approximately 10% of

the cell population. In the ΔminCBs strain producing MinCEc (IB1159) even without xylose addition, the cells became more elongated than the parental strain, with an average cell length of 4.4 μm (Fig. 2b). When xylose was added, the average cell lengths increased to 4.8 μm ABC294640 (Fig. 2c). In both these conditions more than 50% of the cells were longer than 4 μm (Table 2). The number of minicells was not changed significantly and represented 9–12% of the cell population. These data imply that the overexpression of MinCEc

can causes inhibition of the cell division in B. subtilis, although it does not complement the deficiency of MinCBs under these conditions. According to previously published data, the minDBs disruption causes a typical minicell phenotype, with DNA-less minicells and short filaments being formed (Levin et al., 1992; Edwards & Errington, 1997; Marston et al., 1998). It was determined Carnitine dehydrogenase here that the average cell length of the filaments was 3.9 μm and that more than 50% of the ΔminDBs cells (IB1056) were longer than 4 μm (Table 2; Fig. 2d). In comparison with ΔminCBs strain, the number of minicells was slightly higher (11–15%). Afterwards, we compared the lengths of the ΔminDBs (IB1056) cells with the lengths of GFP-MinDEc expressed in the ΔminDBs background (IB1104). If GFP-MinDEc was able to complement MinDBs, the cells would become shorter and formation of minicells would be confined. Indeed, without addition of xylose (Fig. 2e) and at a low concentration of xylose (0.05% w/v; Fig. 2f), GFP-MinDEc was able to improve the phenotype of ΔminDBs cells. The average cell length dropped to 3.4 μm and the percentage of cells longer than 4 μm decreased to 28% (without xylose) (Fig. 2e) and 31% (in the presence of 0.05% xylose) (Fig. 2f). However, the minicell formation was not prevented completely, although it decreased to 8–10%. The use of 0.3% xylose increased the average cell length to 4.