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. 2014 Dec 6;14:42. doi: 10.1186/s12861-014-0042-9

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© Hirose et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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IGF-1R/PI3K and Wnt pathways regulate the activation of mTORC1 during fin regeneration. (A) Scheme of inhibitor treatments of rapamycin, LY294002 (a PI3K inhibitor), NVP-ADW742 (an IGF-1R inhibitor), or IWP-2 (a Wnt/β-catenin inhibitor) during fin regeneration. (B-K) Longitudinal sections of DMSO or inhibitors treated wild-type fin regenerates that were immunohistochemically stained with an antibody against p-S6K (green) at 24 (DMSO, n = 6; Rapa, n = 4; LY294002, n = 4; NVP-ADW742, n = 4; IWP-2, n = 5) and 48 hpa (DMSO, n = 6; Rapa, n = 4; LY294002, n = 4; NVP-ADW742, n = 4; IWP-2, n = 4). DAPI fluorescent signal (blue) indicates the presence of nuclei. The activation of S6K was blocked by LY294002, NVP-ADW742, or IWP-2 treatment. Dashed white lines indicate the amputation planes. Scale bars: 100 μm.