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FatJ acts via the Hippo mediator Yap1 to restrict the size of neural progenitor cell pools

Research output: Contribution to journalArticle

  • Nick J Van Hateren
  • Raman M Das
  • Guillaume M Hautbergue
  • Anne-Gaëlle Borycki
  • Marysia Placzek
  • Stuart A Wilson

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Original languageEnglish
Pages (from-to)1893-902
Number of pages10
JournalDevelopment
Volume138
Issue number10
DOIs
Publication statusPublished - May 2011

Abstract

The size, composition and functioning of the spinal cord is likely to depend on appropriate numbers of progenitor and differentiated cells of a particular class, but little is known about how cell numbers are controlled in specific cell cohorts along the dorsoventral axis of the neural tube. Here, we show that FatJ cadherin, identified in a large-scale RNA interference (RNAi) screen of cadherin genes expressed in the neural tube, is localised to progenitors in intermediate regions of the neural tube. Loss of function of FatJ promotes an increase in dp4-vp1 progenitors and a concomitant increase in differentiated Lim1(+)/Lim2(+) neurons. Our studies reveal that FatJ mediates its action via the Hippo pathway mediator Yap1: loss of downstream Hippo components can rescue the defect caused by loss of FatJ. Together, our data demonstrate that RNAi screens are feasible in the chick embryonic neural tube, and show that FatJ acts through the Hippo pathway to regulate cell numbers in specific subsets of neural progenitor pools and their differentiated progeny.

    Research areas

  • Animals, Avian Proteins, Base Sequence, Cadherins, Cell Count, Chick Embryo, Gene Expression Regulation, Developmental, Gene Knockdown Techniques, Neural Stem Cells, Neural Tube, Oligonucleotide Array Sequence Analysis, Phenotype, RNA Interference, RNA, Small Interfering, Signal Transduction

ID: 13086860