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. 2021 May 19;41(20):4378–4391. doi: 10.1523/JNEUROSCI.2537-20.2021

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Copyright © 2021 Beurg et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 6. — Deafness phenotypes in Tmc1 p.D528N and Tmc1 p.W554L. A, Fixed whole mounts of mid-region of cochleae of P30 Tmc1+/+ (top row) and Tmc1 p.D528N/D528N (bottom row) labeled with phalloidin (actin), calbindin28K (cell somas) and merge. Note absence of IHCs and loss of OHCs, and shape changes to OHC hair bundle in mutant. B, Mean ABR thresholds for four P30 mice in wild-type Tmc1+/+, Tmc1 p.D528N/+, and Tmc1 p.D528N/D528N; Tmc2+/+ mice. The similarity of wild type and heterozygote indicates recessive mutation. C, Survival of IHC and OHC (rows 1, 2, and 3) in four P30 mice in Tmc1 p.D528N/D528N; Tmc2+/+ mice. D, ABR thresholds for four P30 mice in wild-type Tmc1+/+, Tmc1 p.W554L/+ at P30 and Tmc1 p.W554L/W554L at P30 and P60 (all on Tmc2+/+ background). This mutation is recessive too. E, Survival of IHC and OHCs in four P30 mice in Tmc1 p.W554L/W554L; Tmc2+/+ mice at P30 and P60. At P60, only OHCs are missing.