ArticlePLoS computational biology2010
Somitogenesis clock-wave initiation requires differential decay and multiple binding sites for clock protein.
Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Spiral waves and vertebrate embryonic handedness.Journal of biosciences · 2018Article
- The kinetics in mathematical models on segmentation clock genes in zebrafish.Journal of mathematical biology · 2018Article
- Spatial gradients of protein-level time delays set the pace of the traveling segmentation clock waves.Development (Cambridge, England) · 2014Article
- Stochastic simulation of notch signaling reveals novel factors that mediate the differentiation of neural stem cells.Journal of computational biology : a journal of computational molecular cell biology · 2014Article
- Article
- Nonlinearity arising from noncooperative transcription factor binding enhances negative feedback and promotes genetic oscillations.Papers in physics · 2014Article
- Topology and dynamics of the zebrafish segmentation clock core circuit.PLoS biology · 2012Article
- Dickkopf1--a new player in modelling the Wnt pathway.PloS one · 2011Article
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Authors and funding
2 authors.
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Abstract
Somitogenesis is a process common to all vertebrate embryos in which repeated blocks of cells arise from the presomitic mesoderm (PSM) to lay a foundational pattern for trunk and tail development. Somites form in the wake of passing waves of periodic gene expression that originate in the tailbud and sweep posteriorly across the PSM. Previous work has suggested that the waves result from a spatiotemporally graded control protein that affects the oscillation rate of clock-gene expression. With a minimally constructed mathematical model, we study the contribution of two control mechanisms to the initial formation of this gene-expression wave. We test four biologically motivated model scenarios with either one or two clock protein transcription binding sites, and with or without differential decay rates for clock protein monomers and dimers. We examine the sensitivity of wave formation with respect to multiple model parameters and robustness to heterogeneity in cell population. We find that only a model with both multiple binding sites and differential decay rates is able to reproduce experimentally observed waveforms. Our results show that the experimentally observed characteristics of somitogenesis wave initiation constrain the underlying genetic control mechanisms.
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