ArticleNature communications2018
Hidden heterogeneity and circadian-controlled cell fate inferred from single cell lineages.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 66 citations in OpenAlex.
- Understanding cell fate decisions with temporal attention.PLoS computational biology · 2026Article
- BESTDR Enables Bayesian Quantification of Mechanism-Specific Drug Responses.Cancer research · 2026Article
- Lineage-resolved lifetime modelling reveals potential quiescence and synchronization among MDA-MB-468 breast cancer cells.Frontiers in cell and developmental biology · 2026Article
- Drug-tolerant persister cells in cancer: bridging the gaps between bench and bedside.Nature communications · 2025Review
- Inheritable cell-states shape drug-persister correlations and population dynamics in cancer cells.PLoS computational biology · 2025Article
- Subtle alteration in transcriptional memory governs the lineage-level cell cycle duration heterogeneities of mammalian cells.iScience · 2025Article
- Cyclo-stationary distributions of mRNA and Protein counts for random cell division times.bioRxiv : the preprint server for biology · 2025Article
- Combining lineage correlations and a small molecule inhibitor to detect circadian control of the cell cycle.iScience · 2025Article
- Genome-scale CRISPR/Cas9 screening reveals the role ofmSphere · 2025Article
- Measuring FOXO Nuclear Shuttling Dynamics by Fluorescence Microscopy.Methods in molecular biology (Clifton, N.J.) · 2025Article
- p53 and p21 dynamics encode single-cell DNA damage levels, fine-tuning proliferation and shaping population heterogeneity.Communications biology · 2023Article
- Daughter cell fate choice instructed preemptively by mother cells facing nutrient limitation.iScience · 2023Article
- Toward a systems-level probing of tumor clonality.iScience · 2023Review
- FOXO nuclear shuttling dynamics are stimulus-dependent and correspond with cell fate.Molecular biology of the cell · 2023Article
- Cell survival following direct executioner-caspase activation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Quantifying cancer cell plasticity with gene regulatory networks and single-cell dynamics.Frontiers in network physiology · 2023Review
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- Cell-Projection Pumping of Fibroblast Contents into Osteosarcoma SAOS-2 Cells Correlates with Increased SAOS-2 Proliferation and Migration, as well as Altered Morphology.Biomolecules · 2021Article
- Multi-omics integration in the age of million single-cell data.Nature reviews. Nephrology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The origin of lineage correlations among single cells and the extent of heterogeneity in their intermitotic times (IMT) and apoptosis times (AT) remain incompletely understood. Here we developed single cell lineage-tracking experiments and computational algorithms to uncover correlations and heterogeneity in the IMT and AT of a colon cancer cell line before and during cisplatin treatment. These correlations could not be explained using simple protein production/degradation models. Sister cell fates were similar regardless of whether they divided before or after cisplatin administration and did not arise from proximity-related factors, suggesting fate determination early in a cell's lifetime. Based on these findings, we developed a theoretical model explaining how the observed correlation structure can arise from oscillatory mechanisms underlying cell fate control. Our model recapitulated the data only with very specific oscillation periods that fit measured circadian rhythms, thereby suggesting an important role of the circadian clock in controlling cellular fates.
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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.