Speaker
Description
Biological pattern formation is often based on non-linear interactions of chemicals and their movement, and reaction-diffusion models are a classic theoretical framework for explaining such patterning. A good example is seen in the root of Arabidopsis thaliana, where each cell commits to one of two fates: trichoblast and atrichoblast. Experimental data reveal a puzzling phenomenon in this system: two core factors in the regulatory network are predominantly transcribed in one cell type, but their proteins accumulate in the opposite cell type – a counter-intuitive observation that challenges classical reaction-diffusion models.
In this work, we use the mutual support model by Savage et al. (2008) as a framework to study a spatially discrete reaction-diffusion system in which protein and mRNA distributions are out of phase, and proteins move between neighbouring cells through plasmodesmata rather than by extracellular diffusion. The model captures a distinctive feature of this system: proteins form immobile complexes acting as sinks, thereby influencing intercellular distribution. Unlike classical activator-inhibitor systems, there is no obvious local activation, raising new questions about the regulatory setup that allows patterned cell fate decisions. We investigate how these properties allow the network to generate and maintain stable spatial patterns and consider how factors such as positional cues and directed nonlinear movement might further refine pattern selection.
