ArticleNature communications2024
Phenotypic heterogeneity follows a growth-viability tradeoff in response to amino acid identity.
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 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Design of the biosensor-dependent coupling system stabilizes the high-synthesis phenotype of cell factory.Nature communications · 2026Article
- Single cell profiling framework reveals metabolic subpopulations as drivers of bioproduction heterogeneity.Nature communications · 2025Article
- Challenges and Opportunities in Smart Biosensing for Biomanufacturing.ACS synthetic biology · 2025Review
- Equivalent Circuit Modeling and Analysis for Microfluidic Electrical Impedance Monitoring of Single-Cell Growth.Biosensors · 2025Article
- Single-cell heterogeneity in ribosome content and the consequences for the growth laws.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
In their natural environments, microorganisms mainly operate at suboptimal growth conditions with fluctuations in nutrient abundance. The resulting cellular adaptation is subject to conflicting tasks: growth or survival maximisation. Here, we study this adaptation by systematically measuring the impact of a nitrogen downshift to 24 nitrogen sources on cellular metabolism at the single-cell level. Saccharomyces lineages grown in rich media and exposed to a nitrogen downshift gradually differentiate to form two subpopulations of different cell sizes where one favours growth while the other favours viability with an extended chronological lifespan. This differentiation is asymmetrical with daughter cells representing the new differentiated state with increased viability. We characterise the metabolic response of the subpopulations using RNA sequencing, metabolic biosensors and a transcription factor-tagged GFP library coupled to high-throughput microscopy, imaging more than 800,000 cells. We find that the subpopulation with increased viability is associated with a dormant quiescent state displaying differences in MAPK signalling. Depending on the identity of the nitrogen source present, differentiation into the quiescent state can be actively maintained, attenuated, or aborted. These results establish amino acids as important signalling molecules for the formation of genetically identical subpopulations, involved in chronological lifespan and growth rate determination.
Indexed as
Identifiers
What Socratic holds
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.