Modulation of Rok membrane dissociation rate triggers Rok planar polarisation during morphogenesis

Sidor CM1, Stevens TJ1, Boulanger J1, Bailey MJ2, Prehoda KE2, Harris TJ3 and Roeper K1

  1. MRC laboratory of Molecular Biology, Cambridge, UK.
  2. Department of Chemistry and Biochemistry at the University of Oregon, USA.
  3. Department of Cell & Systems Biology, University of Toronto, Canada.

The MyosinII activator Rok is involved in a variety of morphogenetic processes during embryonic development. We have shown previously in the Drosophila embryonic salivary gland placode that Rok is planar polarised at the tissue boundary through a negative regulation by the apical polarity proteins Crumbs (Crb) and aPKC. Intriguingly, despite Crb, aPKC and Rok being expressed in the whole tissue, this effect is specific to the boundary of the tissue. Using FRAP in embryos expressing endogenously tagged Rok, we find that Rok membrane dissociation rate is lower at the boundary of the tissue, where Crb and aPKC membrane levels are lower. Moreover, aPKC can phosphorylate the Rok membrane association region in vitro, suggesting Rok phosphorylation by aPKC might be responsible for the difference in Rok membrane dissociation rate. Finally, computer simulations show that such differences in Rok membrane dissociation rate are sufficient to explain Rok planar polarisation at the tissue boundary.