Ccno, also known as Cyclin O, is a gene that plays a crucial role in regulating the cell cycle. It is involved in the process of multiciliogenesis, which is essential for the formation of multiple motile cilia. These cilia are important for mucociliary clearance and fluid transport along epithelial surfaces [1,2,4,5,6].

In mouse models, the genetic deletion of Ccno leads to a reduced number of multiple motile cilia. This is caused by compromised generation of centrioles at deuterosomes, which are the major amplification platform for centrioles in multiciliated cells (MCCs). Ccno -deficient MCCs fail to sufficiently generate deuterosomes, resulting in only a reduced number of fully functional centrioles that can mature into ciliary basal bodies. These mice also exhibit characteristic phenotypes of MCC dysfunction, such as severe hydrocephalus and mucociliary clearance deficits [6].

In conclusion, Ccno is a key regulator in the transcriptional regulation of multiciliogenesis. Its deficiency in mouse models reveals its importance in the formation of motile cilia and associated physiological functions. Mutations in Ccno in humans are linked to primary ciliary dyskinesia (PCD), a genetically heterogeneous disorder characterized by abnormal ciliary motility, which can lead to severe respiratory diseases, infertility, and other clinical manifestations [1,2,3,4,5].