Investigating auditory transduction functions of myosin VII in Drosophila melanogaster

In a quest to better understand hereditary human deafness we focus on the motor protein myosin VIIA (MyoVIIA), mutations in which underlie dysfunctions in auditory, vestibular and visual processes. Proposed MyoVIIA inner ear functions include tethering transduction channels, trafficking proteins and anchoring hair cell stereocilia by associating with adherens junctions. Fueled by the interest to expand our knowledge of MyoVIIA actions in mechanotransduction we focus on its Drosophila melanogaster homologue, Crinkled (Ck). Drosophila’s auditory organ, Johnston’s Organ (JO), is evolutionarily related to the vertebrate auditory organ. Electrophysiology indicates that Ck is necessary for JO transduction. Microscopy shows apically detached JO transduction units (scolopidia), disrupting stimulus propagation to scolopidia in ck mutants. A scolopidial component (the dendritic cap) is malformed in the absence of Ck and is most likely responsible for detachment. Antibody labeling, rescue and dominant negative experiments establish Ck as functionally necessary in JO cells. While Ck is enriched near cell junctions, it is not necessary for their integrity or the localization of β-catenin, a junctional component. Moreover, Ck is not necessary for localizing TRPV channel subunits or NompA, a dendritic cap component. When we inactivate ck rescue in adult flies, we find that Ck is important for maintaining JO organization. Furthermore, we show that Ck is important for JO