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Control of cranial ectomesenchyme fate by Nr2f nuclear receptors

ABSTRACT: Control of cranial ectomesenchyme fate by Nr2f nuclear receptors

PROVIDER: PRJNA852585 | ENA |

REPOSITORIES: ENA

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Control of cranial ectomesenchyme fate by Nr2f nuclear receptors

Project description:Certain cranial neural crest cells are uniquely endowed with the ability to make skeletal cell types otherwise only derived from mesoderm. As these cells migrate into the pharyngeal arches, they downregulate neural crest specifier genes and upregulate so-called ectomesenchyme genes characteristic of skeletal progenitors. While both external and cell-autonomous factors have been proposed as triggers of this transition, the details remain obscure. Here we report the Nr2f nuclear receptors as novel intrinsic activators of the ectomesenchyme program: zebrafish nr2f5 and nr2f2; nr2f5 mutants show a marked delay in upregulation of ectomesenchyme genes such as dlx2a, prrx1a/b, sox9a, twist1a, and fli1a, and in downregulation of the non-ectomesenchyme specifier sox10. Depending on genotype, mutants partially or fully recover, likely via functional redundancy with other Nr2f genes. Loss of sox10 fully rescued skeletal development in nr2f5 single but not nr2f2; nr2f5 double mutants, while the ectomesenchyme defect persisted in both. Sox10 perdurance thus antagonizes the recovery rather than causing the initial aberration. Unraveling the mechanics of Nr2f function will help solve the enduring puzzle of how cranial neural crest acquire skeletal potency.

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Project description:Purpose: The cranial suture is a fibrous joint, and similar to the growth plates of the skeletal long bone, they serve as the major centers of calvarial vault morphogenesis. Our group’s identification of a skeletal stem cell isolated from the mouse tibial growth plate prompted us to investigate whether these skeletal stem cells are also resident in the mouse cranial sutures and if they govern postnatal suture patency or fusion. Results: We preformed a spatio-temporal profiling of the mouse cranial sutures by flow cytometry, demonstrating a significant decrease in the temporal representation of skeletal stem cells in fusing versus patent sutures. Moreover, canonical Wnt signaling has a significant impact on skeletal stem cells proliferation and thus representation within the suture, dictating fate: fusion or patency. Breeding an Axin2+/-LacZ mouse, with enhanced activation of canonical Wnt signaling to a Twist1+/− mouse, harboring a coronal craniosynostosis enriched the skeletal stem cell pool in coronal sutures, thereby preventing Twist1+/− craniosynostosis. Conclusions: Our findings suggest an imbalance and/or decrease in resident skeletal stem cells within the cranial sutures gives rise to craniosynostosis, however, restoring this representation by enriching skeletal stem cells within the suture can maintain patency.

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