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. 2015 Feb 1;26(3):554–568. doi: 10.1091/mbc.E14-10-1469

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© 2015 Mageswaran 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 1: — ESCRT-II binding partners and their role in endosomal localization and function of ESCRT-II. All strains in this figure lack the genomic copy of VPS36. Tagged versions of wild-type (WT) or mutant copies of VPS36 are expressed from a low-copy CEN plasmid under native promoter. (A) A schematic of ESCRT-II domain architecture, interacting partners, and point mutations used in this study to disrupt these interactions. (B) Endosomal localization of ESCRT-II by fluorescence microscopy and its quantification. Microscopic images are presented in inverted gray scale, where black denotes GFP signal. The GFP puncta represent endosomes since they colocalized with FM4-64 as shown in Supplemental Figure S1C. n = 552, 544, 545, 558, 521, and 461 (in the order of strain presentation). Error bars denote the 95% confidence intervals over mean. N.D., not determined. (C) Localization of GFP-Cps1 in different vps36-mutant strains. (D) Growth assays on plates containing different concentrations of canavanine.