Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux
Issue Date
2013-02-01Author
Khan, Liakot A.
Zhang, Hongjie
Abraham, Nessy
Sun, Lei
Fleming, John T.
Buechner, Matthew
Hall, David H.
Gobel, Verena
Publisher
Nature Publishing Group
Type
Article
Article Version
Scholarly/refereed, author accepted manuscript
Metadata
Show full item recordAbstract
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.
Description
This is the author's accepted manuscript, it is also available here, http:dx.doi.org/10.1038/ncb2656.
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Citation
Khan, Liakot A., Zhang, Hongjie., Abraham, Nessy., Sun, Lei., Fleming, John T., Buechner, Matthew., Hall, David H., Gobel, Verna. "Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux." Nature Cell Biology. January 20, 2013. http:dx.doi.org/10.1038/ncb2656.
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