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

Liakot A. Khan, Hongjie Zhang, Nessy Abraham, Lei Sun, John T. Fleming, Matthew Buechner, David H. Hall, Verena Gobel

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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.

Original languageEnglish (US)
Pages (from-to)143-156
Number of pages14
JournalNature Cell Biology
Volume15
Issue number2
DOIs
StatePublished - Feb 1 2013

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ASJC Scopus subject areas

  • Cell Biology

Cite this

Khan, L. A., Zhang, H., Abraham, N., Sun, L., Fleming, J. T., Buechner, M., Hall, D. H., & Gobel, V. (2013). Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux. Nature Cell Biology, 15(2), 143-156. https://doi.org/10.1038/ncb2656