UMMS Affiliation
Program in Molecular Medicine; Department of Physiology
Publication Date
2008-11-03
Document Type
Article
Disciplines
Life Sciences | Medicine and Health Sciences
Abstract
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.
Rights and Permissions
Copyright remains with the authors.
DOI of Published Version
10.1083/jcb.200808137
Source
J Cell Biol. 2008 Nov 3;183(3):377-84. Link to article on publisher's site.
Journal/Book/Conference Title
The Journal of cell biology
Related Resources
PubMed ID
18981227
Repository Citation
Jonassen JA, San Agustin JT, Follit JA, Pazour GJ. (2008). Deletion of IFT20 in the mouse kidney causes misorientation of the mitotic spindle and cystic kidney disease.. GSBS Student Publications. https://doi.org/10.1083/jcb.200808137. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/1588