74
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      aPKC Phosphorylation of Bazooka Defines the Apical/Lateral Border in Drosophila Epithelial Cells

      research-article
      1 , 1 , 2 , 1 ,
      Cell
      Cell Press
      DEVBIO, CELLBIO

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          Bazooka (PAR-3), PAR-6, and aPKC form a complex that plays a key role in the polarization of many cell types. In epithelial cells, however, Bazooka localizes below PAR-6 and aPKC at the apical/lateral junction. Here, we show that Baz is excluded from the apical aPKC domain in epithelia by aPKC phosphorylation, which disrupts the Baz/aPKC interaction. Removal of Baz from the complex is epithelial-specific because it also requires the Crumbs complex, which prevents the Baz/PAR-6 interaction. In the absence of Crumbs or aPKC phosphorylation of Baz, mislocalized Baz recruits adherens junction components apically, leading to a loss of the apical domain and an expansion of lateral. Thus, apical exclusion of Baz by Crumbs and aPKC defines the apical/lateral border. Although Baz acts as an aPKC targeting and specificity factor in nonepithelial cells, our results reveal that it performs a complementary function in positioning the adherens junction in epithelia.

          Abstract

          Graphical Abstract

          Highlights

          ► aPKC phosphorylates Bazooka to prevent its binding to aPKC ► Crumbs outcompetes phospho-Baz for binding to PAR-6 in epithelial cells ► This mechanism defines the apicial/lateral boundary in epithelia ► Failure to exclude Baz from the aPKC complex disrupts epithelial morphogenesis

          Related collections

          Most cited references54

          • Record: found
          • Abstract: found
          • Article: not found

          Analysis of genetic mosaics in developing and adult Drosophila tissues.

          T Xu, G Rubin (1993)
          We have constructed a series of strains to facilitate the generation and analysis of clones of genetically distinct cells in developing and adult tissues of Drosophila. Each of these strains carries an FRT element, the target for the yeast FLP recombinase, near the base of a major chromosome arm, as well as a gratuitous cell-autonomous marker. Novel markers that carry epitope tags and that are localized to either the cell nucleus or cell membrane have been generated. As a demonstration of how these strains can be used to study a particular gene, we have analyzed the developmental role of the Drosophila EGF receptor homolog. Moreover, we have shown that these strains can be utilized to identify new mutations in mosaic animals in an efficient and unbiased way, thereby providing an unprecedented opportunity to perform systematic genetic screens for mutations affecting many biological processes.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The PAR proteins: fundamental players in animal cell polarization.

            The par genes were discovered in genetic screens for regulators of cytoplasmic partitioning in the early embryo of C. elegans, and encode six different proteins required for asymmetric cell division by the worm zygote. Some of the PAR proteins are localized asymmetrically and form physical complexes with one another. Strikingly, the PAR proteins have been found to regulate cell polarization in many different contexts in diverse animals, suggesting they form part of an ancient and fundamental mechanism for cell polarization. Although the picture of how the PAR proteins function remains incomplete, cell biology and biochemistry are beginning to explain how PAR proteins polarize cells.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              PTEN-mediated apical segregation of phosphoinositides controls epithelial morphogenesis through Cdc42.

              Formation of the apical surface and lumen is a fundamental, yet poorly understood, step in epithelial organ development. We show that PTEN localizes to the apical plasma membrane during epithelial morphogenesis to mediate the enrichment of PtdIns(4,5)P2 at this domain during cyst development in three-dimensional culture. Ectopic PtdIns(4,5)P2 at the basolateral surface causes apical proteins to relocalize to the basolateral surface. Annexin 2 (Anx2) binds PtdIns(4,5)P2 and is recruited to the apical surface. Anx2 binds Cdc42, recruiting it to the apical surface. Cdc42 recruits aPKC to the apical surface. Loss of function of PTEN, Anx2, Cdc42, or aPKC prevents normal development of the apical surface and lumen. We conclude that the mechanism of PTEN, PtdIns(4,5)P2, Anx2, Cdc42, and aPKC controls apical plasma membrane and lumen formation.
                Bookmark

                Author and article information

                Journal
                Cell
                Cell
                Cell
                Cell Press
                0092-8674
                1097-4172
                30 April 2010
                30 April 2010
                : 141
                : 3
                : 509-523
                Affiliations
                [1 ]The Gurdon Institute and the Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
                Author notes
                []Corresponding author d.stjohnston@ 123456gurdon.cam.ac.uk
                [2]

                Present address: Unité Mixte de Recherche GReD, CNRS UMR 6247/ INSERM U931, Faculté de Médecine, Clermont Université, Clermont-Ferrand 63000, France

                Article
                CELL5038
                10.1016/j.cell.2010.02.040
                2885938
                20434988
                0837eb31-1d8f-42bf-b8bc-978908c49aee
                © 2010 ELL & Excerpta Medica.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 27 August 2009
                : 8 January 2010
                : 23 February 2010
                Categories
                Article

                Cell biology
                cellbio,devbio
                Cell biology
                cellbio, devbio

                Comments

                Comment on this article