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. 2017 Jul 7;7:4845. doi: 10.1038/s41598-017-04936-7

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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EcR functionally interacts with hth + tsh in inducing tissue overgrowth. Adult heads (A,C lateral and A’,C’ dorsal views) and eye discs (B,D) of optix > GFP:hth + tsh + GFP (A,B) and optix > GFP:hth + tsh + EcRB1 (C,D) (note that both genotypes harbor equal number of UAS-transgenes). Co-overexpression of EcRB1 enhances the overgrowth of lateral head cuticle and eye disc tissue. Comparison between eye discs overexpressing a dominant-negative form of the EcRB1 (E: optix > GFP + EcRB1-DN) and the co-overexpression of EcRB1-DN with hth + tsh (F: optix > GFP:hth + tsh + EcRB1-DN). Expression of EcRB1 causes a mild reduction in eye disc size (E). Coexpression of EcRB1-DN suppresses the overgrowth produced by hth + tsh (compare F with B). Discs are stained with anti-GFP (green) and anti-Eya (red) antibodies.