Objective: Human genetic mutations that affect the N-terminal head-domain of the nonmuscle myosin-II (MyoII) molecule can result in nonsyndromic sensorineural hearing loss but the underlying mechanism is unknown. Ultimately, MyoII must be appropriately localized in order to execute endogenous functions. The aim of the current study is to determine whether the head-domain of MyoII regulates in vivo localization of the molecule in living and fixed preparations of the auditory organ. Methods: A genetic/transgenic GAL4-UAS approach was used to selectively drive the expression of zip/MyoII (Drosophila homologue of human nonmuscle MyoII) in Drosophila melanogaster auditory (Johnston's organ) sensory neurons. To follow the distribution of the full-length transgene encoded by MyoII, the N-terminus was fused to green fluorescent protein. Additionally, headless zip/MyoII molecules with and without isoleucine-glutamine or IQ motifs were also expressed in Johnston's organ neurons. Results: Removing the entire head domain of MyoII induced localization in neuronal dendrites while removing only a portion of the head but keeping the IQ motif induced localization in the soma and axons of the neurons. Conclusions: The findings suggest that the head domain regulates in vivo localization of MyoII in auditory neurons.
|Number of pages
|International Journal of Pediatric Otorhinolaryngology
|Published - May 2013
- Nonsyndromic hearing loss
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health