This career transitioning project will provide the opportunity, protected time and training for the PI to learn new techniques to translate findings i otoconia biology obtained by animal research to human cases of benign paroxysmal positional vertigo (BPPV) and other otoconial dysfunction. BPPV is the most common cause of vertigo in humans, but the molecular etiology is unknown. My laboratory has been systematically studying molecular mechanisms of otoconia formation, anchoring and maintenance in mice using protein biochemistry, gene targeting, histology (including ultrastructure), and other molecular and cellular techniques. Building on my prior research experience in mouse genetics, I propose to learn cutting-edge genetic and genomic technologies to identify genetic variants or mutations in otoconial genes that may cause or exacerbate recurrent BPPV in patients, with and without hearing loss. In addition, I will learn linkage analysis using familial BPPV cases. Given the high prevalence and debilitating nature of recurrent BPPV and other otoconial dysfunction, often dually inflicted by age-related hearing loss, these types of genetic and translational studies are overdue.