Non-essentiality of canonical cell division genes in the planctomycete Planctopirus limnophila

Elena Rivas-Marin,Christian Jogler,Stijn H Peeters,Damien P Devos,Laura Van Niftrik,Laura Claret Fernández,Sandra Wiegand

doi:10.1038/s41598-019-56978-8

Abstract

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 ovoid planctomycete bacterium Planctopirus limnophila which divides by budding. We attempted to construct P. limnophila knock-out mutants of the genes coding for the divisome proteins FtsI, FtsK, FtsW and the elongasome protein MreB. Surprisingly, ftsI, ftsW and mreB could be deleted without affecting the growth rate. On the other hand, the conserved ftsK appeared to be essential in this bacterium. In conclusion, the canonical bacterial cell division machinery is not essential in P. limnophila and this bacterium divides via budding using an unknown mechanism.

Highlights

The Z-ring is a quasi-universal element of cytokinesis in bacteria that possess PG and divide by binary fission
This lateral cell wall synthesis is performed by the elongasome, a protein complex formed by MreBCD, RodA, RodZ, PBP1A, PBP2 as well as MurF, MurG and MraY25,26
Despite the punctuated pattern of presence of most of the canonical cell division genes in the planctomycetal genomes, ftsK is conserved across the phylum[17], and semi-quantitative RT-PCR assays showed that it is expressed at the same level throughout the cell cycle, as compared to the control gyrA gene, constitutively expressed in most bacteria (Fig. 1)

Summary

Introduction

The Z-ring is a quasi-universal element of cytokinesis in bacteria that possess PG and divide by binary fission. The gene coding for FtsZ is absent from the genomes of a limited number of bacteria These include pathogenic strains from the Tenericutes, the Chlamydiae, and some symbionts such as the gammaproteobacteria “Candidatus Ruthia magnifica”, “Candidatus Vesicomyosocius okutanii HA” and “Candidatus Carsonella ruddii”, the alphaproteobacterium “Candidatus Hodgkinia cicadicola”, and the bacteroidete “Candidatus Sulcia muelleri”[15]. In most of these cases, the loss of ftsZ might be related to the extreme genome reduction associated with their parasitic or endosymbiotic lifestyle. The ftsZ gene is not found in any of the genomes of the Planctomycetes and Chlamydiae These bacteria display a variety of division modes, suggesting that divergent mechanisms have evolved within this superphylum. The budding mechanism has been studied in depth in yeast cells, the molecular mechanism of bacterial budding remains entirely unknown

Methods

Results

Conclusion