A simple mechanochemical model for calcium signalling in embryonic epithelial cells

DOI10.1007/S00285-019-01333-8MaRDI QIDQ2420451zbMATH OpenOpenAlexWikidataFDO

Authors Yanyan Li

Publication date 6 June 2019

Published in Journal of Mathematical Biology (Search for Journal in Brave)

Copyright license Creative Commons Attribution 4.0 International

Full work available at URL https://arxiv.org/abs/1901.07016

zbMATH Keywords

bifurcationscalcium signallingdynamical systemsembryogenesismechanochemical modelneurulationrelaxation oscillationsstretch-sensitive calcium channels

Mathematics Subject Classification ID

Bifurcation theory for ordinary differential equations (34C23) Relaxation oscillations for ordinary differential equations (34C26) Qualitative investigation and simulation of ordinary differential equation models (34C60) Perturbations, asymptotics of solutions to ordinary differential equations (34E10) Biomedical imaging and signal processing (92C55)

Abstract: Calcium (Ca2+) signalling is one of the most important mechanisms of information propagation in the body. In embryogenesis the interplay between Ca2+ signalling and mechanical forces is critical to the healthy development of an embryo but poorly understood. Several types of embryonic cells exhibit calcium-induced contractions and many experiments indicate that Ca2+ signals and contractions are coupled via a two-way mechanochemical coupling. We present a new analysis of experimental data that supports the existence of this coupling during Apical Constriction in Neural Tube Closure. We then propose a mechanochemical model, building on early models that couple Ca2+ dynamics to cell mechanics and replace the bistable Ca2+ release with modern, experimentally validated Ca2+ dynamics. We assume that the cell is a linear viscoelastic material and model the Ca2+-induced contraction stress with a Hill function saturating at high Ca2+ levels. We also express, for the first time, the "stretch-activation" Ca2+ flux in the early mechanochemical models as a bottom-up contribution from stretch-sensitive Ca2+ channels on the cell membrane. We reduce the model to three ordinary differential equations and analyse its bifurcation structure semi-analytically as the $I{P}_3$ concentration, and the "strength" of stretch activation, $lambda$ vary. The Ca2+ system ($lambda=0$, no mechanics) exhibits relaxation oscillations for a certain range of $I{P}_3$ values. As $lambda$ is increased the range of $I{P}_3$ values decreases, the oscillation amplitude decreases and the frequency increases. Oscillations vanish for a sufficiently high value of $lambda$. These results agree with experiments in embryonic cells that also link the loss of Ca2+ oscillations to embryo abnormalities. The work addresses a very important and understudied question on the coupling of chemical and mechanical signalling in embryogenesis.

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Cited in

(5)

• Stability bounds of a delay visco-elastic rheological model with substrate friction
• Mechanochemical models for calcium waves in embryonic epithelia
• Modelling the coupling between intracellular calcium release and the cell cycle during cortical brain development
• Interaction of the IP\(_{3}\)-Ca\(^{2+}\) and MAPK signaling systems in the \textit{Xenopus} blastomere: A possible frequency encoding mechanism for the control of the \textit{Xbra} gene expression
• Fully mixed finite element methods for the coupling of viscoelasticity and reaction-diffusion models

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