Yap is required for ependymal integrity and is suppressed in LPA-induced hydrocephalus

Raehee Park, Uk Yeol Moon, Jun Young Park, Lucinda J. Hughes, Randy L. Johnson, Seo-Hee Cho and Seonhee Kim ()
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Raehee Park: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine
Uk Yeol Moon: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine
Jun Young Park: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine
Lucinda J. Hughes: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine
Randy L. Johnson: MD Anderson Cancer Research Center, University of Texas
Seo-Hee Cho: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine
Seonhee Kim: Shriners Hospitals Pediatrics Research Center, Temple University Lewis Katz School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Timely generation and normal maturation of ependymal cells along the aqueduct are critical for preventing physical blockage between the third and fourth ventricles and the development of fetal non-communicating hydrocephalus. Our study identifies Yap, the downstream effector of the evolutionarily conserved Hippo pathway, as a central regulator for generating developmentally controlled ependymal cells along the ventricular lining of the aqueduct. Yap function is necessary for proper proliferation of progenitors and apical attachment of ependymal precursor cells. Importantly, an injury signal initiated by lysophosphatidic acid (LPA), an upstream regulator of Yap that can cause fetal haemorrhagic hydrocephalus, deregulates Yap in the developing aqueduct. LPA exposure leads to the loss of N-cadherin concentrations at the apical endfeet, which can be partially restored by forced Yap expression and more efficiently by phosphomimetic Yap. These results reveal a novel function of Yap in retaining tissue junctions during normal development and after fetal brain injury.

Date: 2016
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DOI: 10.1038/ncomms10329

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