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. 2018 Aug 16;11(9):dmm032573. doi: 10.1242/dmm.032573

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© 2018. 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. 4. — Glipr1 and MmpB act as TSGs. (A) Morphological changes associated with the downregulation of Glipr1 during regeneration are shown. The most frequently associated defects were epidermal blisters (white arrowheads) and lack of photoreceptors (red arrowheads). Exposure to Cd caused depigmentation, bloating and the development of dorsal outgrowths, especially in head and trunk fragments (asterisks). (B) Smaller outgrowths developed in Glipr1(RNAi) animals also in the absence of Cd; however, these outgrowths could be resorbed (n=7/21) and healed by the animal (n=4/7 at 21 dpa). (C) The Smed-MmpB phenotype was not affected by Cd exposure. Typical lesions associated with MmpB KD were epidermal blisters (white arrowheads), lack of photoreceptors (red arrowheads), supernumerary photoreceptors (yellow arrowheads) and large outgrowths (asterisks). Animals used for the experiments were starved for 2 weeks prior to use and had a length of 6 mm.