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. 2020 Jan 20;48(6):2880–2896. doi: 10.1093/nar/gkaa012

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© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Late conditional inactivation of Six1 in differentiating hair cells results in both structural polarity and PCP defects of hair-bundles. (A, D) Hair-bindle structure and orientation at P0 was visualized by F-actin (red) and anti-acetylated tubulin (green, for kinocilium). (B–K) SEM images from basal or middle cochlear duct showing surface views of the organ of Corti in Eya1^CreER control and Six1^Cko/Cko mutant. Arrows indicate kinocilium (C–J), which is absent in panel K. (L) Percentage of hair cells from the basal region of the cochlea of control (n = 645; 3 embryos) and Rac1 and CKO (n = 622; 3 embryos) with the indicated stereocilia. *P < 0.05, ** P < 0.01, *** P < 0.001. (M) Graphs showing distribution of hair cell orientation from wild-type and Six1 CKO mutant animals. The orientation of hair cells was determined by measuring the angle formed between the medial-to-lateral axis of the cochlea and the line bisecting the stereociliary bundle from the center of the hair cell to the vertex of the hair-bundle.