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Dynein-mediated transport and membrane trafficking control PAR3 polarised distribution

  1. Julie Jouette
  2. Antoine Guichet  Is a corresponding author
  3. Sandra B Claret  Is a corresponding author
  1. Institut Jacques Monod, CNRS, UMR 7592, Paris Diderot University, France
Research Article
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Cite this article as: eLife 2019;8:e40212 doi: 10.7554/eLife.40212

Abstract

The scaffold protein PAR3 and the kinase PAR1 are essential proteins that control cell polarity. Their precise opposite localisations define plasma membrane domains with specific functions. PAR3 and PAR1 are mutually inhibited by direct or indirect phosphorylations, but their fates once phosphorylated are poorly known. Through precise spatiotemporal quantification of PAR3 localisation in the Drosophila oocyte, we identify several mechanisms responsible for its anterior cortex accumulation and its posterior exclusion. We show that PAR3 posterior plasma membrane exclusion depends on PAR1 and an endocytic mechanisms relying on RAB5 and PI(4,5)P2. In a second phase, microtubules and the dynein motor, in connection with vesicular trafficking involving RAB11 and IKK-related kinase, IKKε, are required for PAR3 transport towards the anterior cortex. Altogether our results point to a connection between membrane trafficking and dynein-mediated transport to sustain PAR3 asymmetry.

Article and author information

Author details

  1. Julie Jouette

    Polarity and Morphogenesis Lab, Institut Jacques Monod, CNRS, UMR 7592, Paris Diderot University, Paris, France
    Competing interests
    The authors declare that no competing interests exist.
  2. Antoine Guichet

    Polarity and Morphogenesis Lab, Institut Jacques Monod, CNRS, UMR 7592, Paris Diderot University, Paris, France
    For correspondence
    antoine.guichet@ijm.fr
    Competing interests
    The authors declare that no competing interests exist.
  3. Sandra B Claret

    Polarity and Morphogenesis Lab, Institut Jacques Monod, CNRS, UMR 7592, Paris Diderot University, Paris, France
    For correspondence
    sandra.claret@ijm.fr
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-7167-510X

Funding

Fondation ARC pour la Recherche sur le Cancer (SLR20130607102)

  • Antoine Guichet

Ligue Contre le Cancer (RS14/75-58)

  • Antoine Guichet

Fondation ARC pour la Recherche sur le Cancer (PJA 20141201756)

  • Antoine Guichet

Fondation ARC pour la Recherche sur le Cancer (PJA 20161204931)

  • Antoine Guichet

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Matthew Freeman, University of Oxford, United Kingdom

Publication history

  1. Received: July 19, 2018
  2. Accepted: January 3, 2019
  3. Accepted Manuscript published: January 23, 2019 (version 1)
  4. Version of Record published: February 1, 2019 (version 2)
  5. Version of Record updated: February 1, 2019 (version 3)

Copyright

© 2019, Jouette et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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