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. Author manuscript; available in PMC: 2010 Apr 28.
Published in final edited form as: Dev Dyn. 2008 Nov;237(11):3305–3312. doi: 10.1002/dvdy.21735

Figure 3.

Figure 3

Expression of LIM-HDs in E18.5 cochlea (A-H) and P6 inner ear (I-P). Each stage was labeled with sidebars. A: ISL1 was down-regulated in hair cells at E18.5, while was maintained in all other cochlear cells. B: ISL2 showed the same expression pattern as in E16.5, with slightly higher expression in hair cells than in other cochlear cells. C: Isl2 in situ hybridization showed the same pattern as shown with immunostaining, including spiral ganglions (SG). D: LHX3 showed the same hair cell expression pattern as in E16.5. E, F and H: Expression of Lhx6, Lhx9 and Lmx1b was similar to their respective expression patterns in E16.5. G: Expression of Lmx1a was maintained in the spiral prominence (SP, arrow) and down-regulated in the marginal cells (MC, arrowhead). I: At P6, ISL1 expression was completely absent in hair cells and most supporting cells, while it was maintained in Hensen cells (HeC) and GER. J: Isl1 in situ hybridization showed the result that matched the immunostaining in 3I with the exception in Hensen cells, which may indicate that the immunostaining had higher sensitivity. K: ISL2 expression was up-regulated in hair cells while was maintained at lower level in supporting cells and GER. L: Isl2 in situ hybridization showed expression patterns nearly identical to that obtained from immunostaining study (3K). M,O: Expression of Lhx3 and 9 in P6 utricle and cochlea. N: Lhx5 expression was in the P6 cochlear hair cells, spiral ganglion neurons and very weakly in the GER. P: Lmx1a expression was significantly down-regulated in the transitional epithelium of utricle (bracket). Scale bar=20μm.