ArticleNature communications2024
Determining the rate-limiting processes for cell division in Escherichia coli.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Bacterial growth rate in populations and single cells.Nature microbiology · 2026Review
- Impact of variability in cell generation times on cell-to-cell variability of protein concentrations.bioRxiv : the preprint server for biology · 2026Article
- Rethinking the plasmid paradox: when plasmid costs do not affect fitness.Frontiers in microbiology · 2026Article
- Essentialome-Wide Multigenerational Imaging Reveals Mechanistic Origins of Cell Growth Laws.bioRxiv : the preprint server for biology · 2025Article
- Standardizing Bacterial Extracellular Vesicle Purification: A Call for Consensus.Journal of microbiology and biotechnology · 2025Review
- Uropathogenic Escherichia coli proliferate as a coccoid morphotype inside human host cells.PLoS biology · 2025Article
- Cyclo-stationary distributions of mRNA and Protein counts for random cell division times.bioRxiv : the preprint server for biology · 2025Article
- Determining the rate-limiting processes for cell division in Escherichia coli.Nature communications · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
A critical cell cycle checkpoint for most bacteria is the onset of constriction when the septal peptidoglycan synthesis starts. According to the current understanding, the arrival of FtsN to midcell triggers this checkpoint in Escherichia coli. Recent structural and in vitro data suggests that recruitment of FtsN to the Z-ring leads to a conformational switch in actin-like FtsA, which links FtsZ protofilaments to the cell membrane and acts as a hub for the late divisome proteins. Here, we investigate this putative pathway using in vivo measurements and stochastic cell cycle modeling at moderately fast growth rates. Quantitatively upregulating protein concentrations and determining the resulting division timings shows that FtsN and FtsA numbers are not rate-limiting for the division in E. coli. However, at higher overexpression levels, they affect divisions: FtsN by accelerating and FtsA by inhibiting them. At the same time, we find that the FtsZ numbers in the cell are one of the rate-limiting factors for cell divisions in E. coli. Altogether, these findings suggest that instead of FtsN, accumulation of FtsZ in the Z-ring is one of the main drivers of the onset of constriction in E. coli at faster growth rates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.