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. 2015 Oct 1;8(10):1279–1293. doi: 10.1242/dmm.020719

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© 2015. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 1. — Malignant ras^V12scrib¹ tumors exhibit a unique gene expression profile. (A) Venn diagram shows marked increase in number of genes whose expression changed ≥1.5-fold relative to control (P<0.05) in the EAD bearing ras^V12scrib¹ (in total 3693 genes) compared with ras^V12 alone (1572 genes). Inhibition of JNK signaling (ras^V12scrib¹bsk^DN) reduced the number of deregulated transcripts to 1583. (B) Blocking JNK activity rescued 63% of deregulated genes (blue) in ras^V12scrib¹ tumors, with rescue defined as ≥1.5-fold change in expression from ras^V12scrib¹ towards control levels. Non-invasive ras^V12scrib¹bsk^DN tumors also exhibited a unique set of genes (8%) regulated in a direction opposite to ras^V12scrib¹ mosaic EAD. (C) Distinct functional GO clusters enriched among genes ectopically expressed (red) or downregulated (green) in ras^V12scrib¹ tumors and among those rescued in ras^V12scrib¹bsk^DN (blue) identified by DAVID. For genes falling into individual GO categories, see supplementary material Table S1.