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, Seonhee Kim

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

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.

Original languageEnglish (US)
Article number10329
JournalNature communications
Volume7
DOIs
StatePublished - Jan 12 2016

ASJC Scopus subject areas

  • General Chemistry
  • General Biochemistry, Genetics and Molecular Biology
  • General Physics and Astronomy

MD Anderson CCSG core facilities

  • Genetically Engineered Mouse Facility
  • Research Animal Support Facility

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