| First Author | Yamada T | Year | 2015 |
| Journal | Neurosci Lett | Volume | 584 |
| Pages | 265-9 | PubMed ID | 25451728 |
| Mgi Jnum | J:218762 | Mgi Id | MGI:5618361 |
| Doi | 10.1016/j.neulet.2014.10.001 | Citation | Yamada T, et al. (2015) Neurogenesis of the spiral ganglion cells in the cochlea requires the transcriptional cofactor TIS21. Neurosci Lett 584:265-9 |
| abstractText | The molecular mechanisms controlling the proliferation and differentiation of spiral ganglion cells (SGCs) in the inner ear are still largely unknown. TIS21 is a transcriptional cofactor that shows antiproliferative, antiapoptotic, and prodifferentiative effects on neural progenitor cells. To investigate the function of TIS21 during SGC development, we analyzed SGC neurogenesis from embryonic day 13.5 (E13.5) to postnatal day 4 (P4) in Tis21-GFP knock-in mice, in which the protein-encoding exon of the Tis21 gene was replaced by EGFP. Through E13.5 to P4, we found fewer SGCs in homozygous Tis21-GFP knock-in mice than in wild-type mice. Our results suggest that TIS21 is required for development of SGCs. Deleting Tis21 may affect progenitor cells or neuroblasts at the beginning of cochlear-vestibular ganglion formation and would consequently lead to a decrease in the number of SGCs. |
