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. 2012 Apr 27;21(15):3356–3365. doi: 10.1093/hmg/dds167

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© The Author 2012. Published by Oxford University Press

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Loss of Rtnl1 causes expansion of ER sheets and increases the ER stress response. (A) KDEL distribution in third-instar larval epidermal cells is reticular in control larvae but more diffuse in Rtnl1 RNAi larvae; distribution of the Golgi marker GM130 is broadly unaffected. Graph shows KDEL staining intensity per cell as a percentage of control levels (n= 4 independent experiments; ns, not significant, P > 0.7). (B) Electron micrographs show increased length of ER sheets in Rtnl1 RNAi epidermal cells compared with controls. Arrowheads, ER sheets; Nuc, nucleus; M, mitochondrion. The graph shows the quantification of ER sheet cross-sectional length (***P < 0.005; n = 3 independent larvae). (C and D) Single-confocal sections of larval epidermal cells (C) and ventral nerve cord (D) show increased ER stress, measured by increased Xbp1::GFP expression in Rtnl1 RNAi larvae compared with controls and quantified in graphs (**P < 0.01, ***P < 0.005; n = 12–16).