Evidence map›Paper›PMID 37689712›Full record

ArticleNature communications2023

Dominance vs epistasis: the biophysical origins and plasticity of genetic interactions within and between alleles.

Xuan Xie, Xia Sun, Yuheng Wang, Ben Lehner, Xianghua Li

Abstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Higher-order epistasis within Pol II trigger loop haplotypes.bioRxiv : the preprint server for biology · 2024
    Article
  8. 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

5 authors.

Xuan XieZhejiang University - University of Edinburgh Institute, Zhejiang University School of Medicine, Haining, 314400, P. R. China.
Xia SunZhejiang University - University of Edinburgh Institute, Zhejiang University School of Medicine, Haining, 314400, P. R. China.
Yuheng WangZhejiang University - University of Edinburgh Institute, Zhejiang University School of Medicine, Haining, 314400, P. R. China.ORCID http://orcid.org/0000-0002-9001-0549
Ben LehnerCenter for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona, 08003, Spain. bl11@sanger.ac.uk.ORCID http://orcid.org/0000-0002-8817-1124
Xianghua LiZhejiang University - University of Edinburgh Institute, Zhejiang University School of Medicine, Haining, 314400, P. R. China. xl5@sanger.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An important challenge in genetics, evolution and biotechnology is to understand and predict how mutations combine to alter phenotypes, including molecular activities, fitness and disease. In diploids, mutations in a gene can combine on the same chromosome or on different chromosomes as a "heteroallelic combination". However, a direct comparison of the extent, sign, and stability of the genetic interactions between variants within and between alleles is lacking. Here we use thermodynamic models of protein folding and ligand-binding to show that interactions between mutations within and between alleles are expected in even very simple biophysical systems. Protein folding alone generates within-allele interactions and a single molecular interaction is sufficient to cause between-allele interactions and dominance. These interactions change differently, quantitatively and qualitatively as a system becomes more complex. Altering the concentration of a ligand can, for example, switch alleles from dominant to recessive. Our results show that intra-molecular epistasis and dominance should be widely expected in even the simplest biological systems but also reinforce the view that they are plastic system properties and so a formidable challenge to predict. Accurate prediction of both intra-molecular epistasis and dominance will require either detailed mechanistic understanding and experimental parameterization or brute-force measurement and learning.

Indexed as

Epistasis, GeneticProtein FoldingAllelesBiophysicsLigandsLigands

Identifiers

PMID37689712
PMCPMC10492795

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Registered trials

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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.