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. 2013 May 29;6(5):1285–1291. doi: 10.1242/dmm.011965

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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 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. 2. — Inhibition of Hsp90 partially restores trabeculae in severe mutants. (A) Zebrafish embryos were treated with levels of 17AAG that did not disrupt the craniofacial skeleton in wild type. (B) Untreated gata3 mutants in the severe background typically lack trabeculae (arrowheads). (C) Hsp90 inhibition partially restored the trabeculae, resulting in the fusion of the palate and posterior neurocranium. (D) 17AAG treatment of severe gata3 mutants significantly increases the number of trabeculae in treated embryos (average=0.95, s.e.m.=0.211, s.d.=0.94, n=20) compared with control, DMSO-treated, embryos (average=0.13, s.e.m.=0.05, s.d.=0.34, n=39). (A–C) Dorsal views of flat-mounted neurocrania, anterior to the left; ep, ethmoid plate; tr, trabeculae.