Neurogenesis of the spiral ganglion cells in the cochlea requires the transcriptional cofactor TIS21. (1st January 2015)

• Record Type: Journal Article
• Authors: Yamada, Takao; Minoda, Ryosei; Miwa, Toru; Ise, Momoko; Takeda, Hiroki; Yumoto, Eiji
• Is Part Of: Neuroscience letters. Volume 584(2015)
• Page Start: 265
• Page End: 269
• Publication Date: 2015-01-01
• Subjects: Spiral ganglion cell -- Inner ear -- Cochlea -- Neurogenesis -- TIS21 -- Development; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2014.10.001
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: We assessed the function of TIS21 at the neurogenesis of spiral ganglion cells. The number of spiral ganglion cells decreased in Tis21-GFP knock-in mice. The development of Rosenthal's canals was inhibited in Tis21-GFP knock-in mice. TIS21 may suppress the cell cycle or neurogenesis of spiral ganglion cells. Abstract: 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.