Evidence map›Paper›PMID 35467080›Full record

ArticleMolecular systems biology2022

Single cell variability of CRISPR-Cas interference and adaptation.

Rebecca E McKenzie, Emma M Keizer, Jochem N A Vink, Jasper van Lopik, Ferhat Büke, Vera Kalkman, Christian Fleck, Sander J Tans, Stan J J Brouns

Abstract read
In one paragraph

Article in Molecular systems biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Molecular kinetics dictate population dynamics in CRISPR-based plasmid defense.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. CRISPR memories in single cells.Molecular systems biology · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Rebecca E McKenzie *Department of Bionanoscience, Delft University of Technology, Delft, The Netherlands.ORCID 0000-0003-3627-5367
Emma M Keizer *Biometris, Department of Mathematical and Statistical Methods, Wageningen University, Wageningen, The Netherlands.
Jochem N A VinkDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.
Jasper van LopikDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.ORCID 0000-0001-6981-1504
Ferhat BükeDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.
Vera KalkmanDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.
Christian FleckFreiburg Center for Data Analysis and Modeling (FDM), Spatial Systems Biology Group, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-6371-4495
Sander J TansDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.
Stan J J BrounsDepartment of Bionanoscience, Delft University of Technology, Delft, The Netherlands.ORCID 0000-0002-9573-1724

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While CRISPR-Cas defence mechanisms have been studied on a population level, their temporal dynamics and variability in individual cells have remained unknown. Using a microfluidic device, time-lapse microscopy and mathematical modelling, we studied invader clearance in Escherichia coli across multiple generations. We observed that CRISPR interference is fast with a narrow distribution of clearance times. In contrast, for invaders with escaping PAM mutations we found large cell-to-cell variability, which originates from primed CRISPR adaptation. Faster growth and cell division and higher levels of Cascade increase the chance of clearance by interference, while slower growth is associated with increased chances of clearance by priming. Our findings suggest that Cascade binding to the mutated invader DNA, rather than spacer integration, is the main source of priming heterogeneity. The highly stochastic nature of primed CRISPR adaptation implies that only subpopulations of bacteria are able to respond quickly to invading threats. We conjecture that CRISPR-Cas dynamics and heterogeneity at the cellular level are crucial to understanding the strategy of bacteria in their competition with other species and phages.

Indexed as

BacteriophagesCRISPR-Cas SystemsAdaptation, PhysiologicalDNAEscherichia coliDNAagent-based simulationssingle-cell analysisspacer acquisitiontime-lapse microscopytype I CRISPR-Cas

Identifiers

PMID35467080
PMCPMC10561596

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.