Several well-conserved molecules, such as the apical kinase aPKC, determine apicobasal epithelial polarity. But how do they influence cell fate determination, particularly in vertebrates, in which the aPKC-Par polarity complex's role in neural cell fate diversification has been controversial?Now, on ,Nancy Papalopulu and colleagues illuminate this issue with their study of Xenopus primary neurogenesis, during which the two cell layers of the frog neural plate adopt different fates - deep, non-polar cells become neurons and superficial, polarised cells remain as progenitors. They show that a membrane-tethered form of aPKC suppresses primary neurogenesis in deep cells,while promoting cell proliferation, effects that are mimicked by a nuclear-localised, activated form of aPKC. Blocking endogenous aPKC with a nuclear, dominant-negative form had the opposite effect: it enhanced neurogenesis. Surprisingly, the researchers detected both endogenous and membrane-tethered aPKC in the nucleus, leading them to propose that aPKC acts as a nuclear cell fate determinant during primary neurogenesis, perhaps by transmitting polarity information from membrane to nucleus.
