Calcium signalling is one of the most important mechanisms of
information propagation in the body. In embryogenesis the interplay between calcium
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 calcium signals and contractions are
coupled via a two-way mechanochemical feedback mechanism. We present a new analysis
of experimental data that supports the existence of this coupling during apical
constriction. We then propose a simple mechanochemical model, building on early
models that couple calcium dynamics to the cell mechanics and we replace the
hypothetical bistable calcium release with modern, experimentally validated calcium
dynamics. We assume that the cell is a linear, viscoelastic material and we model
the calcium-induced contraction stress with a Hill function, i.e. saturating at high
calcium levels. We also express, for the first time, the “stretch-activation”
calcium flux in the early mechanochemical models as a bottom-up contribution from
stretch-sensitive calcium channels on the cell membrane. We reduce the model to
three ordinary differential equations and analyse its bifurcation structure
semi-analytically as two bifurcation parameters vary—the
concentration, and the “strength” of stretch activation,
. The calcium system (
, no mechanics) exhibits relaxation oscillations for a certain
range of
values. As
is increased the range of
values decreases and oscillations eventually vanish at a
sufficiently high value of
. This result agrees with experimental evidence in embryonic cells
which also links the loss of calcium oscillations to embryo abnormalities.
Furthermore, as
is increased the oscillation amplitude decreases but the frequency
increases. Finally, we also identify the parameter range for oscillations as the
mechanical responsiveness factor of the cytosol increases. This work addresses a
very important and not well studied question regarding the coupling between chemical
and mechanical signalling in embryogenesis.