PMC:4570552 / 34602-36033 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4570552","sourcedb":"PMC","sourceid":"4570552","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4570552","text":"Figure 4 In Vivo Impact of Aymé-Gripp Syndrome- and Isolated Cataract-Causing MAF Mutations on the Integrity of the Central Nervous System Using a Zebrafish Model\n(A) Dorsal views of uninjected zebrafish embryos (left), and embryos injected with the Aymé-Gripp syndrome-causing mutant (c.161C\u003eT; p.Ser54Leu) (middle) and wild-type (right) MAF capped mRNA (100 pg) at 3 days after fertilization (dpf). Embryos were whole-mount stained using a primary antibody against acetylated tubulin (1:1000, T7451 [Sigma-Aldrich]) that marks neuronal axons, and an Alexa Fluor goat anti-mouse IgG secondary antibody (1:1000, A21207, Invitrogen). The circle highlights the area of the optic tectum that was measured.\n(B) Overexpression of wild-type MAF or the congenital cataracts-causing (c.863G\u003eC; p.Arg288Pro) allele do not induce a significant reduction in the size of the optic tectum. By contrast, overexpression of each of the Aymé-Gripp syndrome-causing alleles results in a statistically significantly reduction of the size of the optic tectum (p \u003c 0.0001). Bars indicate SE, and AU denotes arbitrary units. Statistical analysis was performed using two-tailed Student’s t test. For the measurements performed, we scored 86 control embryos, 61 embryos injected with wild-type MAF mRNA, and 58–70 embryos with each of the Aymé-Gripp syndrome-causing alleles’ mRNA. All experiments were performed blind to injection cocktail in duplicate.","divisions":[{"label":"label","span":{"begin":0,"end":8}},{"label":"p","span":{"begin":10,"end":163}},{"label":"p","span":{"begin":164,"end":703}}],"tracks":[]}