ArticlePLoS computational biology2007
Animal cell differentiation patterns suppress somatic evolution.
Article in PLoS computational biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed.
- DNA methylation in invertebrate genomes and cell lineage plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The dark side of stemness - the role of hematopoietic stem cells in development of blood malignancies.Frontiers in oncology · 2024Review
- Article
- Trade-off between reducing mutational accumulation and increasing commitment to differentiation determines tissue organization.Nature communications · 2022Article
- Constrained optimization of divisional load in hierarchically organized tissues during homeostasis.Journal of the Royal Society, Interface · 2022Article
- Review
- Does Shoot Apical Meristem Function as the Germline in Safeguarding Against Excess of Mutations?Frontiers in plant science · 2021Review
- The evolution of metapopulation dynamics and the number of stem cells in intestinal crypts and other tissue structures in multicellular bodies.Evolutionary applications · 2020Review
- Optimizing homeostatic cell renewal in hierarchical tissues.PLoS computational biology · 2018Article
- Hypothesis: Cancer Is a Disease of Evolved Trade-Offs Between Neoplastic Virulence and Transmission.Journal of Cancer · 2018Review
- Cancer and intercellular cooperation.Royal Society open science · 2017Review
- Hierarchical tissue organization as a general mechanism to limit the accumulation of somatic mutations.Nature communications · 2017Article
- Article
- Cancer across the tree of life: cooperation and cheating in multicellularity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Robustness of differentiation cascades with symmetric stem cell division.Journal of the Royal Society, Interface · 2014Article
- Exploitation of adaptive evolution in glioma treatment.CNS oncology · 2013Review
- An evolutionary explanation for the presence of cancer nonstem cells in neoplasms.Evolutionary applications · 2013Article
- Peto's paradox revisited: theoretical evolutionary dynamics of cancer in wild populations.Evolutionary applications · 2013Article
- Cancer in light of experimental evolution.Current biology : CB · 2012Review
- Clonal analysis reveals multiple functional defects of aged murine hematopoietic stem cells.The Journal of experimental medicine · 2011Article
Corrections and comments
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Authors and funding
3 authors.
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Abstract
Cell differentiation in multicellular organisms has the obvious function during development of creating new cell types. However, in long-lived organisms with extensive cell turnover, cell differentiation often continues after new cell types are no longer needed or produced. Here, we address the question of why this is true. It is believed that multicellular organisms could not have arisen or been evolutionarily stable without possessing mechanisms to suppress somatic selection among cells within organisms, which would otherwise disrupt organismal integrity. Here, we propose that one such mechanism is a specific pattern of ongoing cell differentiation commonly found in metazoans with cell turnover, which we call "serial differentiation." This pattern involves a sequence of differentiation stages, starting with self-renewing somatic stem cells and proceeding through several (non-self-renewing) transient amplifying cell stages before ending with terminally differentiated cells. To test the hypothesis that serial differentiation can suppress somatic evolution, we used an agent-based computer simulation of cell population dynamics and evolution within tissues. The results indicate that, relative to other, simpler patterns, tissues organized into serial differentiation experience lower rates of detrimental cell-level evolution. Self-renewing cell populations are susceptible to somatic evolution, while those that are not self-renewing are not. We find that a mutation disrupting differentiation can create a new self-renewing cell population that is vulnerable to somatic evolution. These results are relevant not only to understanding the evolutionary origins of multicellularity, but also the causes of pathologies such as cancer and senescence in extant metazoans, including humans.
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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.