Fig. 6. Cell proliferation in the developing inner ear is affected by the loss of Hmx2. A-F show the morphological alteration of the Hmx2^lacZ–/– inner ear at E11.5 and E12.0 by examining ß-galactosidase activity. Arrows indicate the presumptive fusion plate that is undergoing thinning and invagination. E and F are sections dorsal to C and D, respectively. The approximate level of sectioning is also indicated in Fig. 2. G-L are the comparable anti-BrdU-labeled sections showing the reduced rate of cell proliferation in the developing Hmx2^lacZ–/– inner ears. Genotypes and embryonic stages are indicated at the top of each column. Control corresponds to either Hmx2^lacZ+/+ or Hmx2^lacZ+/– genotypes. Overt morphological differences can be seen at E11.5 when the invagination of epithelial cells around the posterolateral boundary of the otic vesicle is delayed in the homozygotes (A and B). At E12.0, the close apposition of epithelial walls to form the fusion plates was not present in the otocyst of the Hmx2^lacZ–/– embryo (C,D,E,F). Both the epithelial cells and underlying periotic mesenchymal cells of the corresponding regions are undergoing reduced cell proliferation (J and L). M-P show the apoptotic activities of the otic epithelial cells in the control and Hmx2^lacZ–/– inner ears at E11.5 and E12.0. Arrows indicate the regions of the fusion plates. A higher percentage of cells in the fusion plates are undergoing programmed cell death relative to other regions in both control and Hmx2^lacZ–/– embryos. However, the Hmx2^lacZ–/– otic vesicles do not show an altered rate of cell death relative to the corresponding regions in the control embryos. L, lateral; R, rostral.