ArticleCell2024
A synthetic differentiation circuit in Escherichia coli for suppressing mutant takeover.
Article in Cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Synthetic circuits for cell ratio control.Nature · 2026Article
- Cell cycle criticality as a mechanism for robust cell population control.Molecular systems biology · 2026Article
- Tuning evolvability via plasmid copy number and regulatory architecture.Nature communications · 2025Article
- Programmable cell differentiation in budding yeast uncouples reproductive and metabolic tasks.bioRxiv : the preprint server for biology · 2025Article
- Disentangling Metabolite Detection from Pathway Stress Using Biosensors.ACS synthetic biology · 2025Article
- Transcription regulation by RNA-induced structural strain in duplex DNA.Nucleic acids research · 2025Article
- Preventing Multimer Formation in Commonly Used Synthetic Biology Plasmids.ACS synthetic biology · 2025Article
- Tuning and functionalization of logic gates for time resolved programming of bacterial populations.Nucleic acids research · 2025Article
- LowTempGAL: a highly responsive low temperature-inducible GAL system in Saccharomyces cerevisiae.Nucleic acids research · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiation is crucial for multicellularity. However, it is inherently susceptible to mutant cells that fail to differentiate. These mutants outcompete normal cells by excessive self-renewal. It remains unclear what mechanisms can resist such mutant expansion. Here, we demonstrate a solution by engineering a synthetic differentiation circuit in Escherichia coli that selects against these mutants via a biphasic fitness strategy. The circuit provides tunable production of synthetic analogs of stem, progenitor, and differentiated cells. It resists mutations by coupling differentiation to the production of an essential enzyme, thereby disadvantaging non-differentiating mutants. The circuit selected for and maintained a positive differentiation rate in long-term evolution. Surprisingly, this rate remained constant across vast changes in growth conditions. We found that transit-amplifying cells (fast-growing progenitors) underlie this environmental robustness. Our results provide insight into the stability of differentiation and demonstrate a powerful method for engineering evolutionarily stable multicellular consortia.
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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 OpenQuestion graph.