Histone deacetylase 1 and 2 are essential for murine neural crest proliferation, pharyngeal arch development, and craniofacial morphogenesis

Developmental Dynamics - Tập 246 Số 12 - Trang 1015-1026 - 2017
Zachary J. Milstone1,2, Grace Lawson1, Chinmay M. Trivedi1,2,3
1Cardiovascular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts
2Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts
3Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts

Tóm tắt

Background: Craniofacial anomalies involve defective pharyngeal arch development and neural crest function. Copy number variation at 1p35, containing histone deacetylase 1 (Hdac1), or 6q21‐22, containing Hdac2, are implicated in patients with craniofacial defects, suggesting an important role in guiding neural crest development. However, the roles of Hdac1 and Hdac2 within neural crest cells remain unknown. Results: The neural crest and its derivatives express both Hdac1 and Hdac2 during early murine development. Ablation of Hdac1 and Hdac2 within murine neural crest progenitor cells cause severe hemorrhage, atrophic pharyngeal arches, defective head morphogenesis, and complete embryonic lethality. Embryos lacking Hdac1 and Hdac2 in the neural crest exhibit decreased proliferation and increased apoptosis in both the neural tube and the first pharyngeal arch. Mechanistically, loss of Hdac1 and Hdac2 upregulates cyclin‐dependent kinase inhibitors Cdkn1a, Cdkn1b, Cdkn1c, Cdkn2b, Cdkn2c, and Tp53 within the first pharyngeal arch. Conclusions: Our results show that Hdac1 and Hdac2 function redundantly within the neural crest to regulate proliferation and the development of the pharyngeal arches by means of repression of cyclin‐dependent kinase inhibitors. Developmental Dynamics 246:1015–1026, 2017. © 2017 Wiley Periodicals, Inc.

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Developmental Dynamics

Tập 246 Số 12

1015-1026

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