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ER–endosome contact sites in endosome positioning and protrusion outgrowth

Raiborg, Camilla, Wenzel, Eva M., Pedersen, Nina M., Stenmark, Harald·2016·Biochemical Society Transactions
DOI 10.1042/bst20150246
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Abstract

The endoplasmic reticulum (ER) makes abundant contacts with endosomes, and the numbers of contact sites increase as endosomes mature. It is already clear that such contact sites have diverse compositions and functions, but in this mini-review we will focus on two particular types of ER–endosome contact sites that regulate endosome positioning. Formation of ER–endosome contact sites that contain the cholesterol-binding protein oxysterol-binding protein-related protein 1L (ORP1L) is coordinated with loss of the minus-end-directed microtubule motor Dynein from endosomes. Conversely, formation of ER–endosome contact sites that contain the Kinesin-1-binding protein Protrudin results in transfer of the plus-end-directed microtubule motor Kinesin-1 from ER to endosomes. We discuss the possibility that formation of these two types of contact sites is coordinated as a ‘gear-shift’ mechanism for endosome motility, and we review evidence that Kinesin-1-mediated motility of late endosomes (LEs) to the cell periphery promotes outgrowth of neurites and other protrusions.

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Metadata

Authors
Raiborg, C., Wenzel, E. M., Pedersen, N. M., & Stenmark, H.
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2016-04-11
Volume
44
Issue
2
Pages
441-446
ISSN
  • 0300-5127
  • 1470-8752
DOI
10.1042/bst20150246
Cited by
29
References
0
Language
en

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