KIF26A regulates the development and function of the main olfactory epithelium in mice

Kinesins, which are motor proteins that primarily move along microtubules by hydrolyzing adenosine triphosphate (ATP), constitute a superfamily of proteins known as kinesin superfamily proteins (KIFs). These molecules play crucial roles not only in intracellular transport but also in cell division, cell survival, morphogenesis, and higher brain functions such as memory, learning, and neural network formation. We previously reported that KIF26A plays a key role in the development of the enteric nervous system of the colon. Here, we demonstrate that KIF26A plays a role in olfaction. Analysis of Kif26a^-/- mice reveals that Kif26a is critical for the development of the neuronal layer in the main olfactory epithelium (MOE). At postnatal day 7, Kif26a^-/- mice exhibit decreased thickness and disorganization of the MOE with disproportionate numbers of mature and immature olfactory sensory neurons (OSNs). Loss of KIF26A leads to increased apoptosis and accelerated precursor cell proliferation of OSNs. Additionally, in vitro experiments using primary cultures of neurons reveal that KIF26A deficiency impaired neurite outgrowth and disrupted nerve bundle formation in OSNs. Furthermore, Kif26a haploinsufficiency results in impaired olfactory responses. These findings suggest that KIF26A plays important roles in both olfactory epithelium development and olfactory function.