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Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux
Khan, Liakot A. Zhang, Hongjie Abraham, Nessy Sun, Lei Fleming, John T. Buechner, Matthew Hall, David H. Gobel, Verena
Khan, Liakot A.
Zhang, Hongjie
Abraham, Nessy
Sun, Lei
Fleming, John T.
Buechner, Matthew
Hall, David H.
Gobel, Verena
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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.
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This is the author's accepted manuscript, it is also available here, http:dx.doi.org/10.1038/ncb2656.
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2013-02-01
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Nature Publishing Group
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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.