Table 1.

Loss of neuroD1 function in the neurog1−/− mutants is able to rescue the hair cell defects

AMPMRatio AM/PMn
WT controls19.2 ± 3.117.1 ± 2.61.1315
neurog1−/− controls21.8 ± 1.827.5 ± 30.7916
WT MO–neuroD117.9 ± 1.712.6 ± 1.961.4520 of 33
neurog1−/− MO–neuroD119 ± 419.5 ± 518 of 26
  • Quantification of the AM and PM hair cells at 48 hpf in different embryos: tg[Brn3c:GFP]neurog1+/+, tg[Brn3c:GFP]neurog1−/−, and tg[Brn3c:GFP]neurog1−/− coinjected with MO–neuroD1 and MO–p53. Note that the phenotype displayed by tg[Brn3c:GFP]neurog1−/− in the PM (supernumerary hair cells) is rescued in 30% (8 of 26) of the embryos injected with MO–neuroD1. See that AM/PM = 1 in tg[Brn3c:GFP]neurog1−/− MO–neuroD1-injected embryos (similar to WT AM/PM = 1.13) compared with the non-injected ones (AM/PM = 0.79).