Evidence map›Paper›PMID 22434912›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Geometry, epistasis, and developmental patterning.

Francis Corson, Eric Dean Siggia

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Generative epigenetic landscapes map the topology and topography of cell fates.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Reconstructing Waddington's landscape from data.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Searching for physical principles of morphogenesis.Development (Cambridge, England) · 2025
    Review
  7. Article
  8. Article
  9. A thermodynamic perspective on mammalian neural crest ingression.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Dynamical systems of fate and form in development.Seminars in cell & developmental biology · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Information content and optimization of self-organized developmental systems.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Latent space of a small genetic network: Geometry of dynamics and information.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

2 authors.

Francis CorsonCenter for Studies in Physics and Biology, The Rockefeller University, New York, NY 10021, USA.
Eric Dean Siggia

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Developmental signaling networks are composed of dozens of components whose interactions are very difficult to quantify in an embryo. Geometric reasoning enumerates a discrete hierarchy of phenotypic models with a few composite variables whose parameters may be defined by in vivo data. Vulval development in the nematode Caenorhabditis elegans is a classic model for the integration of two signaling pathways; induction by EGF and lateral signaling through Notch. Existing data for the relative probabilities of the three possible terminal cell types in diverse genetic backgrounds as well as timed ablation of the inductive signal favor one geometric model and suffice to fit most of its parameters. The model is fully dynamic and encompasses both signaling and commitment. It then predicts the correlated cell fate probabilities for a cross between any two backgrounds/conditions. The two signaling pathways are combined additively, without interactions, and epistasis only arises from the nonlinear dynamical flow in the landscape defined by the geometric model. In this way, the model quantitatively fits genetic experiments purporting to show mutual pathway repression. The model quantifies the contributions of extrinsic vs. intrinsic sources of noise in the penetrance of mutant phenotypes in signaling hypomorphs and explains available experiments with no additional parameters. Data for anchor cell ablation fix the parameters needed to define Notch autocrine signaling.

Indexed as

Epistasis, GeneticAnimalsBody PatterningCaenorhabditis elegansCaenorhabditis elegans ProteinsCell LineageCrosses, GeneticEpidermal Growth FactorFemaleMaleModels, BiologicalMutationSignal TransductionVulvaCaenorhabditis elegans ProteinsEpidermal Growth Factor

Identifiers

PMID22434912
PMCPMC3326455

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.