Cell polarisation in a bulk-surface model can be driven by both classic and non-classic Turing instability

摘要

(a)The mechanism described as an expanded activator–inhibitor system. The GTPase Cdc42 is shuffled between its active state A (green) corresponding to the GTP-bound form and its inactive state I (orange) corresponding to the GDP-bound form. Also, the GDI-bound form G (blue) is restricted to the cytosol and is transported to the membrane which corresponds to the influx of inactive form I. The reaction mechanism is determined by three classes of reactions: (1) Flux of inactive Cdc42 over the membrane, (2) Activation and inactivation reactions restricted to the membrane determined by GEFs and GAPs respectively and (3) The positive feedback loop mediated by PAKs and Scaffolds also restricted to the membrane. (b)Geometric domain. By letting the membrane thickness shrink to zero, the geometric description is simplified to one domain Ω corresponding to the cytosol and one boundary Γ corresponding to the membrane. (c)Biological details of Cdc42 activation. Cdc42 has an inhibited GDI-bound form (blue), an inactive GDP-bound form (orange) and an active GTP-bound form (green). The shuffling between these forms is determined by the three regulators namely GDI, GEFs and GAPs. The active form of Cdc42, unlike the inactive, can bind to various effector molecules such as PAKs and Scaffolds which can further bind to GEFs which enhances the activation reaction through a positive feedback loop. This sub panel is re-drawn based on schematic representations in9,25.