Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 30, Pages E3129-E3138Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1404988111
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Funding
- Fonds de la Recherche Scientifique Medicale Grant [3.4550.11]
- Belgian National Fund for Scientific Research Grant [T0002.13]
- Actions de Recherches Concertees Grant [ARC-10/15-026]
- Fondation medicale Reine Elisabeth grant
- Fondation JED-Belgique grant
- Desordres Inflamatoires dans les Affections Neurologiques grant
- Welbio grant from the Region wallonne
- Inter-University Poles of Attraction Grant [PAI P7/20]
- Belgian National Fund for Scientific Research
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In the nervous system, cilia dysfunction perturbs the circulation of the cerebrospinal fluid, thus affecting neurogenesis and brain homeostasis. A role for planar cell polarity (PCP) signaling in the orientation of cilia (rotational polarity) and ciliogenesis is established. However, whether and how PCP regulates cilia positioning in the apical domain (translational polarity) in radial progenitors and ependymal cells remain unclear. By analysis of a large panel of mutant mice, we show that two PCP signals are operating in ciliated cells. The first signal, controlled by cadherin, EGF-like, laminin G-like, seven-pass, G-type receptor (Celsr) 2, Celsr3, Frizzled3 (Fzd3) and Van Gogh like2 (Vangl2) organizes multicilia in individual cells (single-cell polarity), whereas the second signal, governed by Celsr1, Fzd3, and Vangl2, coordinates polarity between cells in both radial progenitors and ependymal cells (tissue polarity). Loss of either of these signals is associated with specific defects in the cytoskeleton. Our data reveal unreported functions of PCP and provide an integrated view of planar polarization of the brain ciliated cells.
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