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. 2013 Jun 1;24(11):1676–1687. doi: 10.1091/mbc.E12-10-0772

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© 2013 Dui 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 3: — Tissue-specific knockdown of dSkp2 causes developmental defects. (A, A′, and A′′) Rough eyes induced by dSkp2 knockdown in the eye (with the use of the ey-Gal4 driver). Results from two independent RNAi lines are shown. (B′, B′′) nub-Gal4-driven expression of these two dSkp2 RNAi lines in the entire wing results in a similar wing hair spacing phenotype (WHS; see the text for details). Control is shown in B. (C′, C′′) dSkp2 knockdown in the posterior region of the wing (driven by en-Gal4) leads to the WHS phenotype in the posterior region only. This phenotype is fully rescued by a simultaneous overexpression of HA-dSkp2 (C).