Expression of Neurog1 instead of Atoh1 can partially rescue organ of Corti cell survival.

ABSTRACT: In the mammalian inner ear neurosensory cell fate depends on three closely related transcription factors, Atoh1 for hair cells and Neurog1 and Neurod1 for neurons. We have previously shown that neuronal cell fate can be altered towards hair cell fate by eliminating Neurod1 mediated repression of Atoh1 expression in neurons. To test whether a similar plasticity is present in hair cell fate commitment, we have generated a knockin (KI) mouse line (Atoh1(KINeurog1)) in which Atoh1 is replaced by Neurog1. Expression of Neurog1 under Atoh1 promoter control alters the cellular gene expression pattern, differentiation and survival of hair cell precursors in both heterozygous (Atoh1(+/KINeurog1)) and homozygous (Atoh1(KINeurog1/KINeurog1)) KI mice. Homozygous KI mice develop patches of organ of Cor

SUBMITTER: Jahan I 

PROVIDER: S-EPMC3265522 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature