Abstract
In A. tumefaciens, the essential FtsZ protein is located at the growth pole before shifting to the mid-cell right before division. Loss of FtsZ causes a halt in cell separation and lysis of cells. To understand how FtsZ polymerization is regulated to properly localize the FtsZ ring at the mid-cell, we have conducted a systematic characterization of the Min system in A. tumefaciens. Our findings indicate that the Min system is not required for cell survival. Yet, we find that the deletion of either minE or minCDE results in a broad cell size distribution, including an increase in the proportion of short and long cells. We observe that the site of constriction is misplaced in the minE or minCDE deletion strains allowing for short cells to arise from sites of constriction near the cell poles. Remarkably, the short cells are viable and contain DNA. In order to observe chromosome replication and segregation in these strains, YFP-ParB is used as a proxy to track the origin of replication as cells elongate and divide. In the absence of the Min proteins, duplication and segregation of the origin of replication is frequently delayed. Taken together, our data suggest that the Min system contributes to the proper regulation of FtsZ placement and subsequent cell division. Furthermore, the failure to precisely place FtsZ rings at mid-cell in the min mutants impacts other cell cycle features including chromosome segregation.
Highlights
Most bacteria precisely place the site of cell division at or near mid-cell through proper positioning of FtsZ to initiate divisome assembly
Transposons accumulate in the min region of A. tumefaciens during saturating transposon mutagenesis experiments in A. tumefaciens suggesting that the Min system is not required for cell survival (Curtis and Brun, 2014)
Similar to findings in S. meliloti (Cheng et al, 2007) and consistent with a saturating transposon screen in A. tumefaciens suggesting that the min genes are not essential (Curtis and Brun, 2014), we have confirmed that the min genes are not required for cell viability (Figure 1)
Summary
Most bacteria precisely place the site of cell division at or near mid-cell through proper positioning of FtsZ to initiate divisome assembly. FtsZ forms a ring-like structure at or near the mid-cell along the cytoplasmic surface of the inner membrane (Bi and Lutkenhaus, 1991). The FtsZ filaments form a ring-like structure at the future site of cell division and guide other divisome proteins, including peptidoglycan synthases, to the mid-cell (Ma et al, 1996; Sun and Margolin, 1998; Den Blaauwen et al, 1999; Li et al, 2007; Goley et al, 2011). Septal peptidoglycan is synthesized inwards to build the new poles of the daughter cells. Septal peptidoglycan synthesis requires the monofunctional PBP3, the SEDS protein FtsW, and the bifunctional PBP1b (Botta and Park, 1981; Bertsche et al, 2006; Cho et al, 2016)
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