Staphylococcus aureus DivIBis a peptidoglycan‐binding protein that is required for a morphological checkpoint in cell division

Abstract

SummaryBacterial cell division is a fundamental process that requires the coordinated actions of a number of proteins which form a complex macromolecular machine known as the divisome. The membrane-spanning proteins DivIB and its orthologue FtsQ are crucial divisome components in Gram-positive and Gramnegative bacteria respectively. However, the role of almost all of the integral division proteins, including DivIB, still remains largely unknown. Here we show that the extracellular domain of DivIB is able to bind peptidoglycan and have mapped the binding to its β subdomain. Conditional mutational studies show that divIB is essential for Staphylococcus aureus growth, while phenotypic analyses following depletion of DivIB results in a block in the completion, but not initiation, of septum formation. Localisation studies suggest that DivIB only transiently localises to the division site and may mark previous sites of septation. We propose that DivIB is required for a molecular checkpoint during division to ensure the correct assembly of the divisome at midcell and to prevent hydrolytic growth of the cell in the absence of a completed septum.

Splitsville: structural and functional insights into the dynamic bacterial Z ring

“…FtsB and FtsL are by themselves unstable in both E. coli and B. subtilis (FtsB is called DivIC in the latter species), but together they associate into a stable complex 83–85 associated with FtsQ (DivIB in B. subtilis and other Gram positives ). Interestingly, the extracellular domain of S. aureus DivIB can bind peptidoglycan 86 despite lacking a binding domain typical of other divisome proteins such as FtsN (see next section). The precise role of this binding, however, is unclear.…”

Isobaric Tags for Relative and Absolute Quantitation Proteomics Analysis of Gene Regulation by SprC in Staphylococcus Aureus

“…SpoIIIE, a homolog of the Bacillus subtilis (45.9% identity) along with FtsK, operates in independent pathways for correcting chromosome segregation during cell division [40,41]. DivIB is necessary for a molecular checkpoint to guarantee the correct assembly of the bacterial divisome which is a macromolecular machine formed by a variety of proteins [42]. Notably, the growth curve of N315ΔsprC mutant did not obviously change when compared with that of wild-type N315 strain, indicating that the effects of DivIB and SpoIIIE's differential expression in this study were inadequate for influencing the proliferation of S. aureus.…”

CozEa and CozEb play overlapping and essential roles in controlling cell division in Staphylococcus aureus

“…Cell division in spherical S. aureus occurs in three consecutive planes, where every new round of division is orthogonal to the previous division plane (Pinho et al, ). Many key cell division proteins known from other model bacteria are conserved in S. aureus , including FtsZ, FtsA, EzrA, GpsB, DivIB, DivIC, FtsL, MurJ, DivIVA, MreC and MreD (Pinho and Errington, ; Pinho and Errington, ; Steele et al, ; Pinho et al, ; Bottomley et al, ; Monteiro et al, ). These proteins are in different ways involved in formation of the division ring and for ensuring proper cell wall synthesis and cell division.…”