  The concept of internal anatomical asymmetry is familiar; usually in humans
the heart is on the left and the liver is on the right, however how does the
developing embryo know to produce this consistent laterality? Symmetry breaking
initiates with left-right asymmetric cilia-driven fluid mechanics in a small
fluid-filled structure called the ventral node in mice. However the question of
what converts this flow into left-right asymmetric development remains
unanswered. A leading hypotheses is that flow transports morphogen containing
vesicles within the node, the absorption of which results in asymmetrical gene
expression. To investigate how vesicle transport might result in the situs
patterns observed in wildtype and mutant experiments, we extend the open source
Stokes flow package, NEAREST, to consider the hydrodynamic and Brownian motion
of particles in a mouse model with flow driven by one, two, and 112 beating
cilia. Three models for morphogen-containing particle released are simulated to
assess their compatibility with observed results in oligociliated and wildtype
mouse embryos: uniformly random release, localised cilium stress induced
release, and localised release from motile cilia themselves. Only the uniformly
random release model appears consistent with the data, with neither
localised-release model resulting in significant transport in the oligociliated
embryo.
