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. 2021 Apr 16;9:649830. doi: 10.3389/fcell.2021.649830

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Copyright © 2021 Landin Malt, Clancy, Hwang, Liu, Smith, Smith, Hatley, Clemens and Lu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Gsk3β inactivation but not Rac1 activation partially rescued cochlear outgrowth of Wls^cKO mutant. (A–F) Dissected cochlear ducts from E18.5 wild-type control (A), Rac1DA/+ (B), Gsk3β^cKO (C), Wls^cKO (D), Wls^cKO; Rac1DA/+ (E), and Wls^cKO; Gsk3β^cKO (F) mutants. (G–L) Flat-mounted OC from the middle region (40–60% cochlear length) of wild-type control (G), Rac1DA/+ (H), Gsk3β^cKO (I), Wls^cKO (J), Wls^cKO; Rac1DA/+ (K), and Wls^cKO; Gsk3β^cKO (L) cochleae stained by phalloidin. Arrowheads indicate the inner pillar cell row. Lateral is up. Scale bars: (A–F), 1 mm; (G–L), 6 μm. (M–O) Quantifications of cochlear length (M), cochlear duct width (N), and presence of extra OHC rows (O) in genotypes indicated by the color keys. Cochlear duct width (N) was not significantly different in all pair-wise comparisons. The number of cochleae analyzed is indicated. Ns, not significant.