Journal
DEVELOPMENT
Volume 139, Issue 5, Pages 968-978Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.065326
Keywords
Adhesion; Cochlea; Planar cell polarity; Mouse
Categories
Funding
- National Institutes of Health [RO1 DC007423, DC005213]
- Natural Science Foundation of China (NSFC) [81028003/H1305, 81000413/H1305]
- Shanghai Rising-Star Program [11QA1401100]
- Research Fund for the Doctoral Program of High Education [20110071120086]
- Neuronal Imaging Core of the Emory Neuroscience National Institute of Neurological Disorders and Stroke (NINDS) [P30NS055077]
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The vertebrate planar cell polarity (PCP) pathway consists of conserved PCP and ciliary genes. During development, the PCP pathway regulates convergent extension (CE) and uniform orientation of sensory hair cells in the cochlea. It is not clear how these diverse morphogenetic processes are regulated by a common set of PCP genes. Here, we show that cellular contacts and geometry change drastically and that the dynamic expression of N-cadherin and E-cadherin demarcates sharp boundaries during cochlear extension. The conditional knockout of a component of the adherens junctions, p120-catenin, leads to the reduction of E-cadherin and N-cadherin and to characteristic cochlear CE defects but not misorientation of hair cells. The specific CE defects in p120-catenin mutants are in contrast to associated CE and hair cell misorientation defects observed in common PCP gene mutants. Moreover, the loss-of-function of a conserved PCP gene, Vangl2, alters the dynamic distribution of N-cadherin and E-cadherin in the cochlea and causes similar abnormalities in cellular morphology to those found in p120-catenin mutants. Conversely, we found that Pcdh15 interacts genetically with PCP genes to regulate the formation of polar hair bundles, but not CE defects in the cochlea. Together, these results indicate that the vertebrate PCP pathway regulates CE and hair cell polarity independently and that a p120-catenin-dependent mechanism regulates CE of the cochlea.
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