Literature DB >> 15456726

Requirement for Par-6 and Bazooka in Drosophila border cell migration.

Elaine M Pinheiro1, Denise J Montell.   

Abstract

Polarized epithelial cells convert into migratory invasive cells during a number of developmental processes, as well as when tumors metastasize. Much has been learned recently concerning the molecules and mechanisms that are responsible for generating and maintaining epithelial cell polarity. However, less is known about what becomes of epithelial polarity proteins when various cell types become migratory and invasive. Here, we report the localization of several apical epithelial proteins, Par-6, Par-3/Bazooka and aPKC, during border cell migration in the Drosophila ovary. All of these proteins remained asymmetrically distributed throughout migration. Moreover, depletion of either Par-6 or Par-3/Bazooka by RNAi resulted in disorganization of the border cell cluster and impaired migration. The distributions of several transmembrane proteins required for migration were abnormal following Par-6 or Par-3/Bazooka downregulation, possibly accounting for the migration defects. Taken together, these results indicate that cells need not lose apical/basal polarity in order to invade neighboring tissues and in some cases even require such polarity for proper motility.

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Year:  2004        PMID: 15456726     DOI: 10.1242/dev.01412

Source DB:  PubMed          Journal:  Development        ISSN: 0950-1991            Impact factor:   6.868


  49 in total

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5.  Cytokine exocytosis and JAK/STAT activation in the Drosophila ovary requires the vesicle trafficking regulator α-Snap.

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Review 6.  Polarity in mammalian epithelial morphogenesis.

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Review 7.  Sticking together the Crumbs - an unexpected function for an old friend.

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Review 8.  Cell motility in cancer invasion and metastasis: insights from simple model organisms.

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9.  Antagonistic functions of Par-1 kinase and protein phosphatase 2A are required for localization of Bazooka and photoreceptor morphogenesis in Drosophila.

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Review 10.  Polarity proteins as regulators of cell junction complexes: implications for breast cancer.

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