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. 2011 Aug 15;22(16):2886–2899. doi: 10.1091/mbc.E10-10-0862

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© 2011 Bernadskaya et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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Figure 7: — A developmental model for the role of Arp2/3 and ERM-1 in apical junction formation during development. Cross–sections of the intestinal tube are shown in developing wild-type and Gex embryos. Polarization of intestinal cells requires the assembly of the apical domain, including apical localization of the junctions, ERM-1, the WAVE/SCAR complex, and F-actin. ERM-1 helps to establish the apical region by binding to cortical F-actin before the apical junctions have fully formed, by localizing WAVE/SCAR apically, and by repositioning the apical junction proteins apicolaterally. When Arp2/3 is present the correct levels of ERM-1 accumulate at the apical plasma membrane, and junctional proteins can accumulate at their correct apicolateral locations. In the absence of Arp2/3 or its activator, the WAVE/SCAR complex, ERM-1 levels are highly elevated. The elevated ERM-1 may displace junctional proteins from the apical domain, leading to decreased junctional proteins at the membrane, less apical F-actin, and an expanded lumen width. Taken together, these defects result in a cell that is only partially polarized.