ArticleNature communications2023
Stochastic gene expression and environmental stressors trigger variable somite segmentation phenotypes.
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.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Early pre-symptomatic and sex-specific cardiac remodeling precedes heart failure in zebrafish with a human actin variant.Disease models & mechanisms · 2026Article
- A genetic modifier links integrin α5 to the phenotypic variation in fibronectin 1a mutant zebrafish.PLoS genetics · 2025Article
- Dual genetic tracing demonstrates the heterogeneous differentiation and function of neuromesodermal progenitors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Simplifications and approximations in a single-gene circuit modeling.Scientific reports · 2024Article
- Stochasticity in genetics and gene regulation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Spatiotemporal control of pattern formation during somitogenesis.Science advances · 2024Review
- Stochastic gene expression and environmental stressors trigger variable somite segmentation phenotypes.Nature communications · 2023Article
- Species-specific roles of the Notch ligands, receptors, and targets orchestrating the signaling landscape of the segmentation clock.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations of several genes cause incomplete penetrance and variable expressivity of phenotypes, which are usually attributed to modifier genes or gene-environment interactions. Here, we show stochastic gene expression underlies the variability of somite segmentation defects in embryos mutant for segmentation clock genes her1 or her7. Phenotypic strength is further augmented by low temperature and hypoxia. By performing live imaging of the segmentation clock reporters, we further show that groups of cells with higher oscillation amplitudes successfully form somites while those with lower amplitudes fail to do so. In unfavorable environments, the number of cycles with high amplitude oscillations and the number of successful segmentations proportionally decrease. These results suggest that individual oscillation cycles stochastically fail to pass a threshold amplitude, resulting in segmentation defects in mutants. Our quantitative methodology is adaptable to investigate variable phenotypes of mutant genes in different tissues.
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Registered trials
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