FatJ acts via the Hippo mediator Yap1 to restrict the size of neural progenitor cell pools
Author(s) -
Nick J. Van Hateren,
Raman M Das,
Guillaume M. Hautbergue,
AnneGaëlle Borycki,
Marysia Placzek,
Stuart A. Wilson
Publication year - 2011
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.064204
Subject(s) - biology , yap1 , progenitor cell , progenitor , microbiology and biotechnology , mediator , neural stem cell , hippo signaling pathway , cell , computational biology , stem cell , genetics , signal transduction , transcription factor , gene
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.
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