| First Author | Hayashi T | Year | 2007 |
| Journal | Dev Dyn | Volume | 236 |
| Issue | 2 | Pages | 525-33 |
| PubMed ID | 17117437 | Mgi Jnum | J:117235 |
| Mgi Id | MGI:3695846 | Doi | 10.1002/dvdy.21026 |
| Citation | Hayashi T, et al. (2007) Loss of Fgfr3 leads to excess hair cell development in the mouse organ of Corti. Dev Dyn 236(2):525-33 |
| abstractText | Previous studies have demonstrated the importance of FGF signaling at several stages in the development of the cochlea. At early stages of embryogenesis, Fgfr1, Fgfr2, and several FGFs are critical for both the induction of the otic vesicle and the initial development of the sensory epithelium. At late stages of cochlear development, Fgfr3 is necessary for the development of the tunnel of Corti. To determine the stage of development when Fgfr3 is required, we examined the expression of Fgfr3 and Fgf8 at various developmental stages. We also re-examined the Fgfr3 -/- mouse with additional markers for developing supporting cells. We confirmed the previous analysis of the Fgfr3 -/- mice, indicating that there are deficiencies in support cell differentiation. Specifically, we find that the inner pillar cell never develops, while the outer pillar cell is stalled in its differentiation. In addition, we found an extra row of outer hair cells, and accompanying Deiters' cells, in the apical two thirds of the organ of Corti in the Fgfr3 mutant. Thus, in addition to controlling the fate decision between pillar cells and Deiters' cells, we find that Fgfr3 also regulates the width of the sensory epithelium. Developmental Dynamics 236:525-533, 2007. (c) 2006 Wiley-Liss, Inc. |
