The divisome at 25: the road ahead

Blaauwen, Tanneke den; Hamoen, Leendert W.; Levin, Petra Anne

doi:10.1016/j.mib.2017.01.007

Cited by 170 publications

(171 citation statements)

References 104 publications

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“…Bacteria multiply by coordinated and essential DNA replication and cell division events, two important biological processes that are valuable targets for antimicrobial therapy (Lock and Harry, ; Adams and Errington, ; Robinson et al , ; Sass and Brötz‐Oesterhelt, ; den Blaauwen et al , ). In the event of DNA damage, the SOS response is activated and ensures that cell division is delayed until the DNA is repaired.…”

Section: Introductionmentioning

confidence: 99%

SosA inhibits cell division in Staphylococcus aureus in response to DNA damage

Bojer

Wacnik

Kjelgaard

et al. 2019

Molecular Microbiology

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Summary Inhibition of cell division is critical for viability under DNA‐damaging conditions. DNA damage induces the SOS response that in bacteria inhibits cell division while repairs are being made. In coccoids, such as the human pathogen, Staphylococcus aureus, this process remains poorly studied. Here, we identify SosA as the staphylococcal SOS‐induced cell division inhibitor. Overproduction of SosA inhibits cell division, while sosA inactivation sensitizes cells to genotoxic stress. SosA is a small, predicted membrane protein with an extracellular C‐terminal domain in which point mutation of residues that are conserved in staphylococci and major truncations abolished the inhibitory activity. In contrast, a minor truncation led to SosA accumulation and a strong cell division inhibitory activity, phenotypically similar to expression of wild‐type SosA in a CtpA membrane protease mutant. This suggests that the extracellular C‐terminus of SosA is required both for cell division inhibition and for turnover of the protein. Microscopy analysis revealed that SosA halts cell division and synchronizes the cell population at a point where division proteins such as FtsZ and EzrA are localized at midcell, and the septum formation is initiated but unable to progress to closure. Thus, our findings show that SosA is central in cell division regulation in staphylococci.

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Section: Introductionmentioning

confidence: 99%

SosA inhibits cell division in Staphylococcus aureus in response to DNA damage

Bojer

Wacnik

Kjelgaard

et al. 2019

Molecular Microbiology

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“…Simultaneously, other proteins, such as the Zap proteins and FtsEX, are recruited to the ring to form the early divisome or protoring. The protoring then recruits the later divisome proteins FtsK, FtsQ, FtsL, FtsB, FtsW, FtsI (PBP3), PBP1b, FtsN (den Blaauwen et al, ), and a number of hydrolases and regulatory proteins (Gray et al, ) to form the mature divisome (Aarsman et al, ). The arrival of FtsN completes the assembly of the core divisome, and signals to initiate septal PG synthesis (Gerding et al, ; Lutkenhaus, ; Weiss, ).…”

Section: Introductionmentioning

confidence: 99%

FtsW activity and lipid II synthesis are required for recruitment of MurJ to midcell during cell division in Escherichia coli

Liu

Meiresonne

Bouhss

et al. 2018

Molecular Microbiology

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Peptidoglycan (PG) is the unique cell shape-determining component of the bacterial envelope, and is a key target for antibiotics. PG synthesis requires the transmembrane movement of the precursor lipid II, and MurJ has been shown to provide this activity in Escherichia coli. However, how MurJ functions in vivo has not been reported. Here we show that MurJ localizes both in the lateral membrane and at midcell, and is recruited to midcell simultaneously with late-localizing divisome proteins and proteins MraY and MurG. MurJ septal localization is dependent on the presence of a complete and active divisome, lipid II synthesis and PBP3/FtsW activities. Inactivation of MurJ, either directly by mutation or through binding with MTSES, did not affect the midcell localization of MurJ. Our study visualizes MurJ localization in vivo and reveals a possible mechanism of MurJ recruitment during cell division.

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“…[64] As mentioned above, FtsZ has multiple spatialr egulators that allow it to coalesce in the form of aZring on the inner membrane at mid-cell (reviewed in Monahan et al [50] ). [64] As mentioned above, FtsZ has multiple spatialr egulators that allow it to coalesce in the form of aZring on the inner membrane at mid-cell (reviewed in Monahan et al [50] ).…”

Section: Ftsz As Ad Ivision Scaffold For Asyncellmentioning

confidence: 99%

Lessons from a Minimal Genome: What Are the Essential Organizing Principles of a Cell Built from Scratch?

et al. 2019

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One of the primary challenges facing synthetic biology is reconstituting a living system from its component parts. A particularly difficult landmark is reconstituting a self‐organizing system that can undergo autonomous chromosome compaction, segregation, and cell division. Here, we discuss how the syn3.0 minimal genome can inform us of the core self‐organizing principles of a living cell and how these self‐organizing processes can be built from the bottom up. The review underscores the importance of fundamental biology in rebuilding life from its molecular constituents.

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The divisome at 25: the road ahead

Cited by 170 publications

References 104 publications

SosA inhibits cell division in Staphylococcus aureus in response to DNA damage

SosA inhibits cell division in Staphylococcus aureus in response to DNA damage

FtsW activity and lipid II synthesis are required for recruitment of MurJ to midcell during cell division in Escherichia coli

Lessons from a Minimal Genome: What Are the Essential Organizing Principles of a Cell Built from Scratch?

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