Khan, LiakotZhang, HongjieAbraham, NessySun, LeiFleming, John T.Buechner, MatthewHall, David H.Gobel, Verena2014-08-132013Khan, Liakot A., Hongjie Zhang, Nessy Abraham, Lei Sun, John T. Fleming, Matthew Buechner, David H. Hall, and Verena Gobel. 2013. “Intracellular lumen extension requires ERM-1-dependent apical membrane expansion and AQP-8-mediated flux.” Nature cell biology 15 (2): 143-156. doi:10.1038/ncb2656. http://dx.doi.org/10.1038/ncb2656.1465-7392http://nrs.harvard.edu/urn-3:HUL.InstRepos:12717502SUMMARY 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 C.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.en-USJournal Article2014-08-1310.1038/ncb2656