1. Cell Biology
  2. Developmental Biology
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The ESCRT Machinery regulates Retromer dependent Transcytosis of Septate Junction Components in Drosophila

  1. Hendrik Pannen
  2. Tim Rapp
  3. Thomas Klein  Is a corresponding author
  1. Heinrich-Heine-Universität Düsseldorf, Germany
Research Article
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Cite this article as: eLife 2020;9:e61866 doi: 10.7554/eLife.61866

Abstract

Loss of ESCRT function in Drosophila imaginal discs is known to cause neoplastic overgrowth fuelled by mis-regulation of signalling pathways. Its impact on junctional integrity, however, remains obscure. To dissect the events leading to neoplasia, we used transmission electron microscopy (TEM) on wing imaginal discs temporally depleted of the ESCRT-III core component Shrub. We find a specific requirement for Shrub in maintaining Septate Junction (SJ) integrity by transporting the Claudin Megatrachea (Mega) to the SJ. In absence of Shrub function, Mega is lost from the SJ and becomes trapped on endosomes coated with the endosomal retrieval machinery Retromer. We show that ESCRT function is required for apical localization and mobility of Retromer positive carrier vesicles, which mediate the biosynthetic delivery of Mega to the SJ. Accordingly, loss of Retromer function impairs the anterograde transport of several SJ core components, revealing a novel physiological role for this ancient endosomal agent.

Data availability

All data generated or analysed during this study are included in the manuscript and supporting files.

Article and author information

Author details

  1. Hendrik Pannen

    Institute of Genetics, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany
    Competing interests
    The authors declare that no competing interests exist.
  2. Tim Rapp

    Institute of Genetics, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany
    Competing interests
    The authors declare that no competing interests exist.
  3. Thomas Klein

    Institute of Genetics, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany
    For correspondence
    thomas.klein@hhu.de
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2719-9617

Funding

Deutsche Forschungsgemeinschaft (Sachbeihilfe KL 1028/11-1)

  • Hendrik Pannen
  • Tim Rapp
  • Thomas Klein

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

Reviewing Editor

  1. Elisabeth Knust, Max-Planck Institute of Molecular Cell Biology and Genetics, Germany

Publication history

  1. Received: August 6, 2020
  2. Accepted: December 29, 2020
  3. Accepted Manuscript published: December 30, 2020 (version 1)
  4. Version of Record published: January 18, 2021 (version 2)

Copyright

© 2020, Pannen 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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