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. 2008 May 19;181(4):697–709. doi: 10.1083/jcb.200801101

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© 2008 Paterson et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 6. — Cortical localization is dependent on both actin and Fus1p. (A and B) Fus2p-GFP localization is disrupted by lat-A in a fus1 mutant. MY9217 was treated with α-factor for 1.5 h and either mock treated or treated with lat-A as in Fig. 5. (A) The fus1 mutation had no effect on the transport or localization of Fus2p-GFP. Arrows indicate rapid movement of Fus2p-GFP dots. (B) Treatment with lat-A (10 min) leads to a rapid loss of Fus2p-GFP localization at the shmoo tip. (C) Texas red–phalloidin staining of fixed cells after lat-A treatment demonstrating actin depolymerization. Bars, 1 μm. (D) Distribution of GFP fluorescence in wild-type and fus1 mutant shmoos. The fraction of total fluorescence was measured for every 1/10 of the cell, starting at the shmoo tip. 50 cells were measured for each strain and condition. Bars represent the mean values; error bars indicate 95% confidence intervals.