Extended Data Fig. 10: Summary of astrocyte self-recognition and morphogenesis via γC3 and chimeric isoform binding.
Astrocyte morphology relies on self-recognition mediated by γC3. Binding between γC3 proteins is likely to activate intracellular signaling pathways which specify distinct morphological consequences. Chimeras which have lost homophilic binding (e.g. M1, M6, M3, and M8) do not promote normal morphogenesis on their own. By contrast, pairs of complementary chimeras (e.g. M1 + M6 and M3 + M8) which bind heterophilically promote normal morphogenesis when expressed in the same astrocyte. The precise mechanism by which γC3 regulates morphogenesis is unclear. Binding could activate repulsion15,48. The initial repulsive response may direct process extension away from sister branches and this would indirectly promote process outgrowth. Alternatively, transient binding between γC3 on opposing processes may directly promote the assembly of signaling complexes which could promote process outgrowth25,44 (see Discussion).
