Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 29, Pages E2996-E3004Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1402105111
Keywords
Cre; anterior commissure; internal capsule; cortical barrels
Categories
Funding
- National Natural Science Foundation of China [31200826, 31070955]
- National Basic Research Program of China [973 Program] [2014CB542205, 2011CB504402]
- Guangdong Natural Science Foundation [S2012040006744]
- Guangzhou Science and Technology Project [13200068]
- Jinan University Research and Innovation Foundation [21612345]
- Belgian grants Actions de Recherches Concertees [ARC-10/15-026]
- Fonds de la Recherche Scientifique Medicale [3.4550.11]
- Fonds National de La Recherche Scientifique (FNRS) [T0002.13]
- Interuniversity Poles of Attraction (Services Federaux des Affaires Scientifiques, Techniques, et Culturelles) [PAI p6/20, PAI7/20]
- Fondation Medicale Reine Elisabeth
- Fondation JED-Belgique
- Region Wallonne [WELBIO-CR-2012A-07]
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Celsr3 and Fzd3, members of core planar cell polarity (PCP) genes, were shown previously to control forebrain axon guidance and wiring by acting in axons and/or guidepost cells. Here, we show that Celsr2 acts redundantly with Celsr3, and that their combined mutation mimics that of Fzd3. The phenotypes generated upon inactivation of Fzd3 in different forebrain compartments are similar to those in conditional Celsr2-3 mutants, indicating that Fzd3 and Celsr2-3 act in the same population of cells. Inactivation of Celsr2-3 or Fzd3 in thalamus does not affect forebrain wiring, and joint inactivation in cortex and thalamus adds little to cortical inactivation alone in terms of thalamocortical projections. On the other hand, joint inactivation perturbs strongly the formation of the barrel field, which is unaffected upon single cortical or thalamic inactivation, indicating a role for interactions between thalamic axons and cortical neurons in cortical arealization. Unexpectedly, forebrain wiring is normal in mice defective in Vangl1 and Vangl2, showing that, contrary to epithelial PCP, axon guidance can be Vangl independent in some contexts. Our results suggest that Celsr2-3 and Fzd3 regulate axonal navigation in the forebrain by using mechanisms different from classical epithelial PCP, and require interacting partners other than Vangl1-2 that remain to be identified.
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