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. 2013 Jan 11;6(3):661–678. doi: 10.1242/dmm.010066

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© 2013. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 8. — Activation of Rok and Myosin II lead to increased expression of the JNK target Mmp1 in EAD clones. Confocal planar apical sections through the epithelium of third instar larval EADs. Mutant clones are marked by the presence of GFP (green). EADs were stained for Mmp1 to reveal JNK activity (white) and with phalloidin-TRITC to detect F-actin (white). (A) rok^CAT. (B) Ras^ACT. (C) rok^CAT + Ras^ACT. (D) sqh^EE. (E) sqh^EE + Ras^ACT. Third instar EADs from rok^CAT mosaic larvae did not show upregulation of Mmp1 in the majority of clones, although expression was mildly induced in some clones (not shown). Expression of Ras^ACT alone did not upregulate Mmp1 in the majority of clones. Mmp1 was strongly upregulated in most rok^CAT + Ras^ACT clones (arrows, C-Cii) compared with adjacent wild-type tissue. Expression of sqh^EE did not lead to Mmp1 upregulation in the clones (D), whereas expression of sqh^EE + Ras^ACT resulted in induction of Mmp1 in many but not all clones (arrows, E-Eii). (F) Quantification of Mmp1 levels in sqh^EE, sqh^EE + Ras^ACT, rok^CAT or rok^CAT + Ras^ACT clones versus wild-type clones. The data was compared by a t-test and error bars represent s.e.m. The significance was P<0.0001 for rok^CAT + Ras^ACT compared with rok^CAT and P<0.08 for sqh^EE + Ras^ACT compared with sqh^EE.