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Pten regulates neural crest proliferation and differentiation during mouse craniofacial development
Author(s) -
Yang Tianfang,
Moore Matthew,
He Fenglei
Publication year - 2018
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.24605
Subject(s) - pten , tensin , neural crest , biology , pi3k/akt/mtor pathway , protein kinase b , craniofacial , microbiology and biotechnology , morphogenesis , cancer research , signal transduction , genetics , embryo , gene
Background: The phosphatase and tensin homolog deleted on chromosome TEN ( Pten ) is implicated in a broad range of developmental events and diseases. However, its role in neural crest and craniofacial development has not been well illustrated. Results: Using genetically engineered mouse models, we showed that inactivating Pten specifically in neural crest cells causes malformation of craniofacial structures. Pten conditional knockout mice exhibit perinatal lethality with overgrowth of craniofacial structures. At the cellular level, Pten deficiency increases cell proliferation rate and enhances osteoblast differentiation. Our data further revealed that inactivating Pten elevates PI3K/Akt signaling activity in neural crest derivatives, and confirmed that attenuation of PI3K/Akt activity led to decreased neural crest cell proliferation and differentiation both in vitro and in vivo. Conclusions: Our study revealed that Pten is essential for craniofacial morphogenesis in mice. Inactivating Pten in neural crest cells increases proliferation rate and promotes their differentiation toward osteoblasts. Our data further indicate that Pten acts via modulating PI3K/Akt activity during these processes. Developmental Dynamics 247:304–314, 2018 . © 2017 Wiley Periodicals, Inc.