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Fig. 5. Knockdown of hace1 by HACE1 MO2 leads to a phenotype similar to that caused by HACE1 MO treatment. a Embryos were injected with 50 ng of Control MO (left panel) or 50 ng of HACE1 MO2 (right panel) into dorsal blastomeres at the four-cell stage and fixed at stage 38/39. Representative results from two independent experiments are shown (Control MO, n = 39; HACE1 MO2, n = 40) (b, c) Embryos were classified into severe, mild, and normal groups on the basis of the extent of each defect. b N, number of total right and left sides of embryos we evaluated. The right side and left side of each embryo were separately evaluated. c N, number of total eyes we evaluated. The right eye and left eye of each embryo were separately evaluated. d, e The body length of embryos at stage 38/39 was quantified (Control MO, n = 39; HACE1 MO2, n = 40). Values are expressed as the mean ± s.d. ***P < 0.001, unpaired t-test. f Embryos were injected with 50 ng of Control MO (left panel) or 50 ng of HACE1 MO2 (right panel) into dorsal blastomeres at the four-cell stage and the images were collected at stage 20 (Control MO, n = 40; HACE1 MO2, n = 40). Anterior views with dorsal to the top Image published in: Iimura A et al. (2016) © The Author(s). This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution license Larger Image Printer Friendly View

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