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Fig. 3. Middle ear and hyoid skeletal changes in tamoxifen-induced Hoxa2 mutant mice. Middle ear (A-H) and hyoid (I-L) skeletal preparations from 18.5 dpc fetuses are shown. (B-G) Hoxa2^flox/flox;Cre-ERT2 homozygous mutant fetuses in the absence (B) and presence (C-G) of TM treatment at different time points from 7.0 dpc up to 11.0 dpc, as indicated. Although untreated Hoxa2^flox/flox;Cre-ERT2 mice have normal middle ear bones (B; compare with Fig. 1D), homeotic duplications comparable to those of the conventional Hoxa2^–/– mutant (A) are observed in C,D. In E-G, the gonial bone (Go, arrow in E) is no longer transformed in fetuses treated from 9.5 dpc onwards, while the remaining cartilage and dermal bone elements are duplicated. By contrast, Hoxa2^flox/flox;Cre-ERT2 fetuses treated at 11.5 dpc (H) do not show any duplication. In H, malformed second arch structures, including stapes (S) and styloid process (St), are often fused to additional ectopic cartilages (arrows), while duplication of dermal bones is not observed. Asterisks in J-L show the loss of the lesser horns (LH) of the hyoid bone in Hoxa2^flox/flox;Cre-ERT2 18.5 dpc fetuses treated at 9.5 dpc (J), 11.0 dpc (K) and 11.5 dpc (L), similar to in conventional Hoxa2^–/– mutants (Fig. 1H). These structures are present in untreated Hoxa2^flox/flox;Cre-ERT2 mice (arrow in I).

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