Skip to main content
. 2012 Nov 14;32(46):16424–16434. doi: 10.1523/JNEUROSCI.3686-12.2012

Figure 2.

Figure 2.

Supernumerary hair cells are produced in the PM in the absence of neurog1 function. Hair cell fate analysis in the maculae of control (A, C) and morphants for neurog1 (B, D) at 48 hpf. tg[Brn3c:mGFP] line was used as a readout of hair cell formation. A–D, Maximal intensity projections of maculae in the otic vesicles of control and morphant embryos. Note that the size of the AM does not change during neurog1 knockdown, but the PM is enlarged (compare red line in C with red–green line in D). E, F, Cristae hair cells are unaffected in morphant embryos. G, H, Single confocal planes of the PM in WT (G) or neurog1−/− (H) embryos in the tg[Brn3c:mGFP] background; note the expansion of the PM in neurog1−/− mutants. I–K, Quantification of hair cells in I, the AM and PM of control and MO–neurog1 embryos at 48 hpf and 3 dpf; J, the ant-PM and post-PM of control and morphant embryos at 48 hpf (note that only the ant-PM region displays an increase in the number of hair cells); K, the AM and PM of WT and neurog1−/− mutants. **p < 0.005 and ***p < 0.001. White circles indicate the contour of the otic vesicle. A,B and E–H, are lateral views with anterior to the left and dorsal to the top. C and D are dorsal views with anterior to the left. ac, Anterior crista; lc, lateral crista; pc, posterior crista; ov, otic vesicle; NM, neuromast; A, anterior; D, dorsal; L, lateral.