作者: Richard Benton , Daniel St Johnston
DOI: 10.1016/S0092-8674(03)00938-3
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摘要: PAR-1 kinases are required for polarity in diverse cell types, such as epithelial cells, where they localize laterally. activity is believed to be transduced by binding of 14-3-3 proteins its phosphorylated substrates, but the relevant targets unknown. We show that phosphorylates Bazooka/PAR-3 on two conserved serines generate sites. This inhibits formation Bazooka/PAR-6/aPKC complex blocking Bazooka oligomerization and aPKC. In epithelia, this localizes apically defines apical membrane, whereas lacking phosphorylation/14-3-3 sites forms ectopic lateral complexes. Lateral exclusion PAR-1/14-3-3 cooperates with anchoring Crumbs/Stardust restrict localization, loss both pathways disrupts polarity. also excludes from posterior oocyte, disruption regulation causes anterior-posterior defects. Thus, antagonism may represent a general mechanism establishing complementary cortical domains polarized cells.