Deletion of IFT20 in the mouse kidney causes misorientation of the mitotic spindle and cystic kidney disease.
Document Type
Journal ArticlePublication Date
2008-11-03Keywords
Animals; Carrier Proteins; Cell Differentiation; Cell Division; Centrosome; Chromosomes, Mammalian; Gene Deletion; Kidney; Kidney Diseases, Cystic; Mice; Mice, Knockout; Mitotic Spindle Apparatus; Wnt ProteinsLife Sciences
Medicine and Health Sciences
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Show full item recordAbstract
Primary cilia project from the surface of most vertebrate cells and are thought to be sensory organelles. Defects in primary cilia lead to cystic kidney disease, although the ciliary mechanisms that promote and maintain normal renal function remain incompletely understood. In this work, we generated a floxed allele of the ciliary assembly gene Ift20. Deleting this gene specifically in kidney collecting duct cells prevents cilia formation and promotes rapid postnatal cystic expansion of the kidney. Dividing collecting duct cells in early stages of cyst formation fail to properly orient their mitotic spindles along the tubule, whereas nondividing cells improperly position their centrosomes. At later stages, cells lacking cilia have increased canonical Wnt signaling and increased rates of proliferation. Thus, IFT20 functions to couple extracellular events to cell proliferation and differentiation.Source
J Cell Biol. 2008 Nov 3;183(3):377-84. Link to article on publisher's site.DOI
10.1083/jcb.200808137Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33038PubMed ID
18981227; 18981227Related Resources
Link to article in PubMedRights
Copyright remains with the authors.ae974a485f413a2113503eed53cd6c53
10.1083/jcb.200808137