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Figure 4


Fig. 4. Deletion of TR{alpha}1 but not TRß exclusively restores KCNQ4 expression in OHCs despite hypothyroidism. (A,C) At P12, in hypothyroid TRß–/– mutants (hypo), KCNQ4 protein was not observed (A), prestin was expressed but its distribution remained immature (C). (B,D) In hypothyroid TR{alpha}1–/– mutants (hypo), KCNQ4 appears normal (B), whereas prestin persists in an immature distribution (D). (E,F) T4-mediated rescue leads to a normal adult expression of KCNQ4 in hypothyroid TRß–/– mutants (E), like in T4-treated TR{alpha}1–/– mutants (F). (G,H) T4 does not rescue prestin from its immature pattern in hypothyroid TRß–/– mutants (G), but does so in hypothyroid TR{alpha}1–/– mutants (H). Sections were coimmunolabeled with synaptophysin (green) and DAPI (blue). Arrows, basal pole of OHC. Bar, 10 µm.





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