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. 2016 Feb 15;30(4):399–407. doi: 10.1101/gad.274134.115

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© 2016 Santanam et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 4. — Autophagy deficiency results in ER stress and decreased AR signaling. (A) One percent methylene blue-stained tissue showing representative areas used for EM analysis. Representative transmission EM (TEM) with ER and mitochondria (M) labeled as well as calreticulin and AR IHC of Atg7^+/+ and Atg7^Δ/Δ anterior mouse prostates at 3 mo after tumor induction. (B) Western blot analysis of pPERK, PERK, p-eIF2α, and eIF2α expression in tumor lysates from Atg7^+/+ and Atg7^Δ/Δ anterior mouse prostates at 3 mo after tumor induction. Tubulin served as a loading control. (C) Quantification of the percentage of cells with AR-positive nuclei in Atg7^+/+ and Atg7^Δ/Δ anterior mouse prostate tissue (n = 2) at various times after tumor induction. The Atg7^+/+ tumors had 88.6% and 81.35% AR-positive nuclei at 3 and 6 mo, respectively, whereas the Atg7^Δ/Δ tumors had only 58.2% and 65.45% positive nuclei at 3 and 6 mo after TAM, respectively. (D) Western blot analysis of AR and IGF-1β expression in Atg7^+/+ and Atg7^Δ/Δ mouse prostates at 3 mo after tumor induction.