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Later at Salk, Kintner focused on the development of cells with motile cilia. Cells extend motile cilia to produce directed fluid flow, which can function in a variety of ways. This activity is most prominent in the lung, where multiciliated cells line the airways and produce a vigorous fluid flow that clears mucus, pathogens and debris. Defects in these cells result from primary ciliary dyskinesia, a disorder in which an inherited genetic mutation causes defects in cilia movement. These multiciliated lung cells are also disrupted in a variety of respiratory ailments brought about by viral infections, smoking or cystic fibrosis.
Kintner’s work in this area showed that the gene FoxJ1 is sufficient to induce cells to form a motile cilium. He later identified a second gene called multicilin that instructs cells to not only turn on Foxj1 and make motile cilia, but also to generate the cilia-nucleating structures, called basal bodies, which allow a cell to form hundreds of cilia. This discovery led to the finding that patients who lack ciliated cells in the lungs have mutations in multicilin. In the future, multicilin could be used to coax stem cells to form new cilia to treat diseases.
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