ArticlePLoS biology2009
Cell lineages and the logic of proliferative control.
Article in PLoS biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 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
161 citing papers in PubMed.
- Synthetic developmental engineering of human liver organogenesis.Development (Cambridge, England) · 2026Review
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- Cell cycle criticality as a mechanism for robust cell population control.Molecular systems biology · 2026Article
- The inherent fragility of collective proliferative control.iScience · 2025Article
- Mechanical control of cell fate decisions in the skin epidermis.Nature communications · 2025Article
- In silico modeling of directed differentiation of induced pluripotent stem cells to definitive endoderm.PLoS computational biology · 2025Article
- Multi-Layer Autocatalytic Feedback Enables Integral Control Amidst Resource Competition and Across Scales.ACS synthetic biology · 2025Article
- A Bayesian phylodynamic inference framework for single-cell CRISPR/Cas9 lineage tracing barcode data with dependent target sites.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Licensing and niche competition in spermatogenesis: mathematical models suggest complementary regulation of tissue maintenance.Development (Cambridge, England) · 2025Article
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- Dynamically adjusted cell fate decisions and resilience to mutant invasion during steady-state hematopoiesis revealed by an experimentally parameterized mathematical model.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A large-scale CRISPR screen reveals context-specific genetic regulation of retinal ganglion cell regeneration.Development (Cambridge, England) · 2024Article
- Tradeoff between speed and robustness in primordium initiation mediated by auxin-CUC1 interaction.Nature communications · 2024Article
- A modelling framework for cancer ecology and evolution.Journal of the Royal Society, Interface · 2024Article
- Tradeoff Between Speed and Robustness in Primordium Initiation Mediated by Auxin-CUC1 Interaction.bioRxiv : the preprint server for biology · 2024Article
- Homeostatic regulation of renewing tissue cell populations via crowding control: stability, robustness and quasi-dedifferentiation.Journal of mathematical biology · 2024Article
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- Feedback control of organ size precision is mediated by BMP2-regulated apoptosis in the Drosophila eye.PLoS biology · 2024Article
- Self-Regulated Symmetry Breaking Model for Stem Cell Differentiation.Entropy (Basel, Switzerland) · 2023Article
- Predictive nonlinear modeling of malignant myelopoiesis and tyrosine kinase inhibitor therapy.eLife · 2023Article
101 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
Abstract
It is widely accepted that the growth and regeneration of tissues and organs is tightly controlled. Although experimental studies are beginning to reveal molecular mechanisms underlying such control, there is still very little known about the control strategies themselves. Here, we consider how secreted negative feedback factors ("chalones") may be used to control the output of multistage cell lineages, as exemplified by the actions of GDF11 and activin in a self-renewing neural tissue, the mammalian olfactory epithelium (OE). We begin by specifying performance objectives-what, precisely, is being controlled, and to what degree-and go on to calculate how well different types of feedback configurations, feedback sensitivities, and tissue architectures achieve control. Ultimately, we show that many features of the OE-the number of feedback loops, the cellular processes targeted by feedback, even the location of progenitor cells within the tissue-fit with expectations for the best possible control. In so doing, we also show that certain distinctions that are commonly drawn among cells and molecules-such as whether a cell is a stem cell or transit-amplifying cell, or whether a molecule is a growth inhibitor or stimulator-may be the consequences of control, and not a reflection of intrinsic differences in cellular or molecular character.
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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.