aPKC, Crumbs3 and Lgl2 control apicobasal polarity in early vertebrate development

In early vertebrate development, apicobasally polarised blastomeres divide to produce inner non-polarised cells and outer polarised cells that follow different fates. How the polarity of these early blastomeres is established is not known. We have examined the role of Crumbs3, Lg12 and the apical aPKC in the polarisation of frog blastomeres. Lg12 localises to the basolateral membrane of blastomeres, while Crumbs3 localises to the apical and basolateral membranes. Overexpression aPKC and Crumbs3 expands the apical domain at the expense of the basolateral and repositions tight junctions in the new apical-basolateral interface. Loss of aPKC function causes loss of apical markers and redirects basolateral markers ectopically to the apical membrane. Cell polarity and tight junctions, but not cell adhesion, are lost and outer polarised cells become inner-like apolar cells. Overexpression of Xenopus Lg12 phenocopies the aPKC knockout, suggesting that Lg12 and aPKC act antagonistically. This was confirmed by showing that aPKC and Lg12 can inhibit the localisation of each other and that Lg12 rescues the apicalisation caused by aPKC. We conclude that an instrumental antagonistic interaction between aPKC and Lg12 defines apicobasal polarity in early vertebrate development.