Evidence map›Paper›PMID 39933591›Full record

ArticleJournal of the Royal Society, Interface2025

Model-guided gene circuit design for engineering genetically stable cell populations in diverse applications.

Kirill Sechkar, Harrison Steel

Abstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Bioengineering hybrid artificial life.Frontiers in bioinformatics · 2025
    Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Kirill SechkarDepartment of Engineering Science, University of Oxford, Parks Road, Oxford OX1 3PJ, UK.ORCID 0000-0003-2300-8278
Harrison SteelDepartment of Engineering Science, University of Oxford, Parks Road, Oxford OX1 3PJ, UK.ORCID 0000-0002-9625-4755

Funding

Engineering and Physical Sciences Research Council
6 · The paper itself

Abstract

Maintaining engineered cell populations' genetic stability is a key challenge in synthetic biology. Synthetic genetic constructs compete with a host cell's native genes for expression resources, burdening the cell and impairing its growth. This creates a selective pressure favouring mutations which alleviate this growth defect by removing synthetic gene expression. Non-functional mutants thus spread in cell populations, eventually making them lose engineered functions. Past work has attempted to limit mutation spread by coupling synthetic gene expression to survival. However, these approaches are highly context-dependent and must be tailor-made for each particular synthetic gene circuit to be retained. By contrast, we develop and analyse a biomolecular controller which depresses mutant cell growth independently of the mutated synthetic gene's identity. Modelling shows how our design can be deployed alongside various synthetic circuits without any re-engineering of its genetic components, outperforming extant gene-specific mutation spread mitigation strategies. Our controller's performance is evaluated using a novel simulation approach which leverages resource-aware cell modelling to directly link a circuit's design parameters to its population-level behaviour. Our design's adaptability promises to mitigate mutation spread in an expanded range of applications, while our analyses provide a blueprint for using resource-aware cell models in circuit design.

Indexed as

Gene Regulatory NetworksGenetic EngineeringModels, GeneticSynthetic BiologyMutationburdengene circuit designmathematical modelpopulationresource competitionsynthetic biology

Identifiers

PMID39933591
PMCPMC11813585

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.