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. 2021 May 28;9:679325. doi: 10.3389/fcell.2021.679325

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Copyright © 2021 Durán Alonso, Vendrell, López-Hernández, Alonso, Martin, Giráldez, Carramolino, Giovinazzo, Vázquez, Torres and Schimmang.

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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Effects of tissue-specific inactivation of Meis2 on inner ear formation. (A,B) lacZ ROSA26 reporter staining caused by the MafBCre driver in the posterior hindbrain of E8.25 embryos and in rhombomeres (r) flanking the otic vesicle at E9 (B). (C–H) Meis2^flox/flox; MafB^Cre/+ mutants show reduced sized vesicles (C,D) which maintain expression of Dlx5 (at E9) and Pax2 (at E9,5), as revealed by whole mount RNA in situ hybridization (E,F) and immunohistochemistry (G,H). The orientations of the sections through the otic vesicles along the dorsal (d)–lateral (l) axis are indicated. (I–L) Bright field view of otic vesicles at E11.5 and cleared inner ears at P1 from Meis2^flox/flox; Foxg1^Cre/+ mutants. Note the flask-shaped morphology of the otic vesicle and the lack of a discernible cochlea (co) in the mutants. v, vestibule.