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Broadly speaking, Gata3 is a transcription factor involved in neurosensory specification and hair cell differentiation. Previous studies have shown that Gata3 null mutants do not develop neurons, so Gata3 appears to be necessary for neuronal survival. To better understand the role of Gata3 in spiral ganglion neurons of the inner ear, a Neurod1-cre model was used to conditionally knock out Gata3 at E9-E9.5, the timepoint when neuroblasts first begin to delaminate from the otic placode. The mutants used in this study were Nd1-cre: Gata3 f/f mutants. In situ was performed to determine gene expression within the cochlea, and immunohistochemistry was performed to label neurons as well as cell death within the cochlea. When Gata3 was conditionally knocked out and reduced in its expression, fewer neurons appear to have formed compared to the mutant and the neurons that do form lack normal projection patterns. Increased Activated Caspase3 labelling was found in the mutant compared to the control, meaning that there was increased cell death in the mutant. The Activated Caspase3 labelling follows the general pathway of the neurons, leading to the belief that neurons were the cells that were dying when Gata3 was conditionally knocked out. Based on this, Gata3 does appear to be necessary for SGN survival within the inner ear.
Ahmad, Hiba, "How Gata3 Affects Neuronal Survival in the Inner Ear" (2021). Honors Theses. 3408.
Honors Thesis-Open Access