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. 2017 Sep 15;144(18):3349–3360. doi: 10.1242/dev.144519

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© 2017. Published by The Company of Biologists Ltd

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Fig. 8. — Overexpression of cNtn1-Myc in mice leads to excess fusion and canal truncations. Paint-fills of E14.5 mouse inner ears. Whereas control Ntn1^CE/+ (A, n=15 ears) and Ntn1^CE/CE (not shown; n=11 ears) mice develop with normal canal morphology, some FoxG1^Cre; Ntn1^CE/+ ears display thinning (not shown; n=5/49 ears) or a complete truncation of the lateral canal (B, arrowhead; n=2/49 ears). Rare anterior (C, arrowhead; n=2/49 ears) and posterior (not shown; n=2/49 ears) defects were also observed. Overall, nine out of 28 animals (32%) showed a defect in at least one ear. Crect; Ntn1^CE/+ ears also show defects in canal morphogenesis, but only in the lateral canal (D,E). Both thinning (D, arrowhead; n=10/34 ears) and complete truncations (E, arrowhead; n=9/34 ears) were observed. The overall distribution of defects is illustrated in F. In this case, 14 out of 20 animals (70%) showed a defect in at least one ear. Scale bar: 500 µm.