Non-essentiality of canonical cell division genes in Planctopirus limnophila (mreB, ftsI, ftsW)

Most bacteria divide by binary fission using an FtsZ-based mechanism that relies on a multi-protein complex, the divisome. In the majority of non-spherical bacteria another multi-protein complex, the elongasome, is also required for the maintenance of cell shape. Components of these multi-protein assemblies are conserved and essential in most bacteria. Here, we provide evidence that at least three proteins of these two complexes are not essential in the FtsZ-less planctomycete bacterium Planctopirus limnophila which divides by budding. We performed P. limnophila knock-out mutants of the genes coding for FtsI, FtsK, FtsW (divisome) and MreB (elongasome). Surprisingly, FtsI, FtsW and MreB could be deleted without apparent phenotype. On the other side, the conserved FtsK appears to be essential in this bacterium. In addition, we show that the mreB inhibitor A22 causes cell division phenotypes in a ΔmreB strain, which questions the specificity of this commonly used drug. In conclusion, the canonical bacterial cell division machinery is not essential in the planctomycete P. limnophila and this bacterium divides via budding using an unknown mechanism