Dr. Hertzano’s research interests are focused on revealing the cell type-specific genetic and genomic regulatory pathways which control inner ear development and its molecular signaling cascades in health and disease. This knowledge is essential not only for the identification of new deafness genes, but can be applied to drive stem cells into desired cell fates for therapeutics. Cell Type-Specific Transcriptional Cascades in Inner Ear Development: one of the missions of the LIEDG is to reveal cell type-specific genetic and genomic regulatory pathways which control inner ear development. To accomplish these goals the team successfully developed and validated protocols for cell type-specific analysis of the ear using fluorescent activated cell sorting, and continues to develop these protocols to extend them to additional cell types and species. For example, using this approach we identified Zeb1 and miR200b as key regulators of epithelial-mesenchymal fate in the mouse inner ear (Hertzano et al. 2011, Kurima et al. 2011), and deciphered the mechanism of a mutation in the Zeb1 gene in the Twirler mutant mouse. Current projects focus on hair cell-specific regulatory pathways important for terminal differentiation and deciphering the molecular mechanisms underlying deafness as a result of mutations in hair cell-expressed transcription factors and miRNAs. Molecular Mechanisms Underlying Acquired Hearing Loss: while congenital hearing loss affects 1 in 1000 newborns, age related hearing loss afflicts that majority of the elderly population and noise induced hearing loss affects 5% of the population world-wide and is a major problem for veterans. In this project the LIEDG is taking a cell type-specific approach to interrogate the translatomes of adult inner ears as they are exposed to noise with and without treatment. Using advanced bioinformatic approaches our goal is to decipher the mechanisms underlying acquired hearing loss to develop targeted therapeutics.