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. 2010 Jan 25;188(2):191–198. doi: 10.1083/jcb.200911102

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© 2010 Holland 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 4. — Phosphorylation of multiple sites is required for optimal Plk4 destruction. (A) Alignment showing the positions of the different phosphorylation mutations in Plk4. Immunoblot showing the relative expression levels of WT, AA, A1, A2, A3, A4, and KD Plk4-EYFP. (B) Graph quantifying of the proportion of cells with more than four centrioles 48 h after induction of Plk4-EYFP. Uninduced samples (−Tet) are shown for comparison. (C) Graph quantifying the mean number of centrioles per cell in cells with more than four centrioles. Counting was performed 48 h after induction of Plk4-EYFP. Uninduced samples are shown for comparison. (D) Immunofluorescence images acquired 48 h after Plk4-EYFP was induced. Insets depict an enlargement of centrioles. Red, SAS-6; green, Plk4-EYFP; blue, DNA. Bars, 10 µm. (E) A model for the autoregulation of Plk4 stability. Bars represent the mean of at least three independent experiments with >300 cells per condition. Error bars represent the SEM.