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Nat Cell Biol. 2013 Feb;15(2):143-56. doi: 10.1038/ncb2656. Epub 2013 Jan 20.

Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux.

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1
Department of Pediatrics, Massachusetts General Hospital, Boston, 02114, USA.

Erratum in

  • Nat Cell Biol. 2013 Mar;15(3):335.

Abstract

Many unicellular tubes such as capillaries form lumens intracellularly, a process that is not well understood. Here we show that the cortical membrane organizer ERM-1 is required to expand the intracellular apical/lumenal membrane and its actin undercoat during single-cell Caenorhabditis elegans excretory canal morphogenesis. We characterize AQP-8, identified in an ERM-1-overexpression (ERM-1[++]) suppressor screen, as a canalicular aquaporin that interacts with ERM-1 in lumen extension in a mercury-sensitive manner, implicating water-channel activity. AQP-8 is transiently recruited to the lumen by ERM-1, co-localizing in peri-lumenal cuffs interspaced along expanding canals. An ERM-1[++]-mediated increase in the number of lumen-associated canaliculi is reversed by AQP-8 depletion. We propose that the ERM-1/AQP-8 interaction propels lumen extension by translumenal flux, suggesting a direct morphogenetic effect of water-channel-regulated fluid pressure.

Comment in

PMID:
23334498
PMCID:
PMC4091717
DOI:
10.1038/ncb2656
[Indexed for MEDLINE]
Free PMC Article
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