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Defective motile cilia in Prickle2-deficient mice.

Authors
  • Sowers, Levi P
  • Yin, Terry
  • Mahajan, Vinit B
  • Bassuk, Alexander G
Type
Published Article
Journal
Journal of Neurogenetics
Publisher
Informa UK (Taylor & Francis)
Publication Date
Jan 01, 2014
Volume
28
Issue
1-2
Pages
146–152
Identifiers
DOI: 10.3109/01677063.2014.885966
PMID: 24708399
Source
Medline
Keywords
License
Unknown

Abstract

Motile cilia play diverse roles across phyla and cell types, and abnormalities in motile cilia lead to numerous disease states, including hydrocephalus. Although motile ciliary abnormalities in Prickle2 mutants have not yet been described, the planar cell polarity genes, including Prickle2, are implicated in the development and function of motile cilia. This report evaluates Prickle2-deficient mice for dysfunction in processes known to depend on functioning motile cilia. Prickle2-deficient mice do not develop hydrocephalus, but do display abnormal morphology and motility in the motile cilia of the ependyma. The morphology of tracheal motile cilia is also abnormal. Taken together, these results demonstrate that Prickle2 is required for normal ependymal motile cilia development and function.

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