Evidence map›Paper›PMID 25024187›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Spatial interactions and cooperation can change the speed of evolution of complex phenotypes.

Natalia L Komarova

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Homeostasis Back and Forth: An Ecoevolutionary Perspective of Cancer.Cold Spring Harbor perspectives in medicine · 2017
    Review
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  15. A population genetics perspective on the determinants of intra-tumor heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
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  19. In the light of evolution VIII: Darwinian thinking in the social sciences. Introduction.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Natalia L KomarovaDepartments of Mathematics and Ecology and Evolutionary Biology, University of California, Irvine, CA 92697 komarova@uci.edu.
University of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complex traits arise from the interactions among multiple gene products. In the case where the complex phenotype is separated from the wild type by a fitness valley or a fitness plateau, the generation of a complex phenotype may take a very long evolutionary time. Interestingly, the rate of evolution depends in nontrivial ways on various properties of the underlying stochastic process, such as the spatial organization of the population and social interactions among cells. Here we review some of our recent work that investigates these phenomena in asexual populations. The role of spatial constraints is quite complex: there are realistic cases where spatial constrains can accelerate or delay evolution, or even influence it in a nonmonotonic fashion, where evolution works fastest for intermediate-range constraints. Social interactions among cells can be studied in the context of the division-of-labor games. Under a range of circumstances, cooperation among cells can lead to a relatively fast creation of a complex phenotype as an emerging (distributed) property. If we further assume the presence of cheaters, we observe the emergence of a fully mutated population of cells possessing the complex phenotype. Applications of these ideas to cancer initiation and biofilm formation in bacteria are discussed.

Indexed as

Evolution, MolecularCell CommunicationCell DivisionGenetic FitnessHomeostasisHumansModels, GeneticMutationNeoplasmsPhenotypeTumor MicroenvironmentTumor Suppressor ProteinsTumor Suppressor Proteinsmutationsstochastic modeling

Identifiers

PMID25024187
PMCPMC4113926
OpenAlexW2081645471

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.