High impact information on Otof

• Exocytosis in Otof(-/-) IHCs is almost completely abolished, despite normal ribbon synapse morphogenesis and Ca(2+) current [1].
• Otoferlin, defective in a human deafness form, is essential for exocytosis at the auditory ribbon synapse [1].
• Otoferlin binds Ca(2+) and displays Ca(2+)-dependent interactions with the SNARE proteins syntaxin1 and SNAP25 [1].
• We show that otoferlin expression in the hair cells correlates with afferent synaptogenesis and find that otoferlin localizes to ribbon-associated synaptic vesicles [1].
• We studied otoferlin, a predicted C2-domain transmembrane protein, which is defective in a recessive form of human deafness [1].

Biological context of Otof

• Thus, otoferlin is essential for a late step of synaptic vesicle exocytosis and may act as the major Ca(2+) sensor triggering membrane fusion at the IHC ribbon synapse [1].

Anatomical context of Otof

• Otoferlin-expressing, Ca(v)1.3 deletion-sensitive outer hair cells in the low frequency range could be clearly separated from otoferlin-negative, BK deletion-sensitive outer hair cells in the high frequency range [2].

References