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Retinoic acid receptors exhibit cell‐autonomous functions in cranial neural crest cells
Author(s) -
Dupé Valérie,
Pellerin Isabelle
Publication year - 2009
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22087
Subject(s) - biology , retinoic acid , neural crest , microbiology and biotechnology , cranial neural crest , retinoic acid receptor , endocrinology , medicine , hindbrain , retinoic acid receptor alpha , anatomy , genetics , embryo , gene
Previous work has emphasized the crucial role of retinoic acid (RA) in the ontogenesis of the vast majority of mesenchymal structures derived from the neural crest cells (NCC), which migrate through, or populate, the frontonasal process and branchial arches. Using somatic mutagenesis in the mouse, we have selectively ablated two or three retinoic acid receptors (i.e., RARα/RARβ, RARα/RARγ and RARα/RARβ/RARγ) in NCC. By rigorously analyzing these mutant mice, we found that survival and migration of NCC is normal until gestational day 10.5, suggesting that RAR‐dependent signaling is not intrinsically required for the early steps of NCC development. However, ablation of Rara and Rarg genes in NCC yields an agenesis of the median portion of the face, demonstrating that RARα and RARγ act cell‐autonomously in postmigratory NCC to control the development of structures derived from the frontonasal process. In contrast, ablation of the three Rar genes in NCC leads to less severe defects of the branchial arches derived structures compared with Rar compound null mutants. Therefore, RARs exert a function in the NCC as well as in a separated cell population. This work demonstrates that RARs use distinct mechanisms to pattern cranial NCC. Developmental Dynamics 238:2701–2711, 2009. © 2009 Wiley‐Liss, Inc.