Radial glial cells (RGCs), which span the entire width of the developing cerebral cortex, act as neural progenitors and provide a polarised scaffold for the migration of newborn neurons. But what are the molecular factors that regulate their polarisation? Eva Anton and co-workers now reveal that in mice,the calmodulin-binding protein MARCKS, a PKC substrate, is involved in this process (see ). In Marcks-/- mice, they report, the RGC scaffold is disrupted. Marcks-/- RGCs proliferate aberrantly and are frequently abnormally localised. The polarised distribution of cell-polarity markers, such as PAR complex proteins, in RGCs is also disrupted, as is RGC-guided neuronal migration, leading to defects in cortical lamination. Surprisingly, the phosphorylation of MARCKS by PKC is not required for its function in RGCs, but its myristoylation-mediated targeting to the plasma membrane is. The authors conclude that myristoylated MARCKS is crucial for RGC development and suggest that MARCKS might serve as an anchor for the membrane localisation of crucial signalling complexes.
