ArticleGenetics2014
Fisher's geometrical model emerges as a property of complex integrated phenotypic networks.
Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed.
- Gene-level complexity explains genome-wide variation in the distribution of fitness effects.Molecular biology and evolution · 2026Article
- Genotype-fitness mapping of adaptive mutants reveals shifting low-dimensional structure across divergent environments.PLoS biology · 2026Article
- Weakest link epistasis and the geometry of genetic load.bioRxiv : the preprint server for biology · 2026Article
- Article
- Effects of inbreeding on balancing selection: insights from Fisher's geometric model.Genetics · 2025Article
- Alternative Mutational Architectures Producing Identical M-Matrices can Lead to Different Patterns of Evolutionary Divergence.Genome biology and evolution · 2025Article
- Lethal mutagenesis and the transient within-host dynamics of viral adaptation.Virus evolution · 2025Article
- Fisher's Geometric Model as a Tool to Study Speciation.Cold Spring Harbor perspectives in biology · 2024Review
- Evolutionary rescue on genotypic fitness landscapes.Journal of the Royal Society, Interface · 2023Article
- A null model for the distribution of fitness effects of mutations.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Host heterogeneity and epistasis explain punctuated evolution of SARS-CoV-2.PLoS computational biology · 2023Article
- The diverse effects of phenotypic dominance on hybrid fitness.Evolution; international journal of organic evolution · 2022Article
- Immune Heterogeneity and Epistasis Explain Punctuated Evolution of SARS-CoV-2.medRxiv : the preprint server for health sciences · 2022Article
- System drift and speciation.Evolution; international journal of organic evolution · 2022Article
- The integrative biology of genetic dominance.Biological reviews of the Cambridge Philosophical Society · 2021Review
- Article
- The geometry and genetics of hybridization.Evolution; international journal of organic evolution · 2020Article
- Multi-locus interactions and the build-up of reproductive isolation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Genetic Paths to Evolutionary Rescue and the Distribution of Fitness Effects Along Them.Genetics · 2020Article
- Recent insights into the genotype-phenotype relationship from massively parallel genetic assays.Evolutionary applications · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Models relating phenotype space to fitness (phenotype-fitness landscapes) have seen important developments recently. They can roughly be divided into mechanistic models (e.g., metabolic networks) and more heuristic models like Fisher's geometrical model. Each has its own drawbacks, but both yield testable predictions on how the context (genomic background or environment) affects the distribution of mutation effects on fitness and thus adaptation. Both have received some empirical validation. This article aims at bridging the gap between these approaches. A derivation of the Fisher model "from first principles" is proposed, where the basic assumptions emerge from a more general model, inspired by mechanistic networks. I start from a general phenotypic network relating unspecified phenotypic traits and fitness. A limited set of qualitative assumptions is then imposed, mostly corresponding to known features of phenotypic networks: a large set of traits is pleiotropically affected by mutations and determines a much smaller set of traits under optimizing selection. Otherwise, the model remains fairly general regarding the phenotypic processes involved or the distribution of mutation effects affecting the network. A statistical treatment and a local approximation close to a fitness optimum yield a landscape that is effectively the isotropic Fisher model or its extension with a single dominant phenotypic direction. The fit of the resulting alternative distributions is illustrated in an empirical data set. These results bear implications on the validity of Fisher's model's assumptions and on which features of mutation fitness effects may vary (or not) across genomic or environmental contexts.
Indexed as
Identifiers
What OpenQuestion holds
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.