ArticlePLoS genetics2018
mTOR acts as a pivotal signaling hub for neural crest cells during craniofacial development.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Identification of Gβ5 Interactome Associated with Neuronal Development in Neuro-2a Cells through miniTurbo Proximity Labeling.ACS omega · 2026Article
- Piezo channels contribute to the terminal cytodifferentiation of odontoblasts via modulation of canonical Wnt signaling.International journal of oral science · 2026Article
- COVID-19 and Congenital Cleft Lip and Palate: A Systematic Review Focusing on Nonsyndromic Neonatal Outcomes.Cureus · 2026Review
- Kdf1 Regulates Molar Cusp Morphogenesis via the PI3K/AKT/mTOR Signalling Axis.Cell proliferation · 2026Article
- Isogenic hiPSC models of Turner syndrome development reveal shared roles of inactive X and Y in the human cranial neural crest network.American journal of human genetics · 2025Article
- Alcohol induces p53-mediated apoptosis in neural crest by stimulating an AMPK-mediated suppression of TORC1, S6K, and ribosomal biogenesis.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Piezo1 and Piezo2 collectively regulate jawbone development.Development (Cambridge, England) · 2024Article
- The level of protein in the maternal murine diet modulates the facial appearance of the offspring via mTORC1 signaling.Nature communications · 2024Article
- Zebrafish raptor mutation inhibits the activity of mTORC1, inducing craniofacial defects due to autophagy-induced neural crest cell death.Development (Cambridge, England) · 2024Article
- Chronic paternal alcohol exposures induce dose-dependent changes in offspring craniofacial shape and symmetry.Frontiers in cell and developmental biology · 2024Article
- Up-Regulation of microRNA-424 Causes an Imbalance in AKT Phosphorylation and Impairs Enteric Neural Crest Cell Migration in Hirschsprung Disease.International journal of molecular sciences · 2023Article
- mTORC1 signaling pathway regulates tooth repair.International journal of oral science · 2023Article
- Activation of Rictor/mTORC2 signaling acts as a pivotal strategy to protect against sensorineural hearing loss.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neural crest metabolism: At the crossroads of development and disease.Developmental biology · 2021Review
- Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic β-catenin degradation.Science signaling · 2021Article
- Deregulated Rac1 Activity in Neural Crest Controls Cell Proliferation, Migration and Differentiation During Midbrain Development.Frontiers in cell and developmental biology · 2021Article
- Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development.Theranostics · 2021Article
- GCN5 acetylation is required for craniofacial chondrocyte maturation.Developmental biology · 2020Article
- Wnt regulates amino acid transporter Slc7a5 and so constrains the integrated stress response in mouse embryos.EMBO reports · 2020Article
- LKB1 specifies neural crest cell fates through pyruvate-alanine cycling.Science advances · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
mTOR is a highly conserved serine/threonine protein kinase that is critical for diverse cellular processes in both developmental and physiological settings. mTOR interacts with a set of molecules including Raptor and Rictor to form two distinct functional complexes, namely the mTORC1 and mTORC2. Here, we used novel genetic models to investigate functions of the mTOR pathway for cranial neural crest cells (NCCs), which are a temporary type of cells arising from the ectoderm layer and migrate to the pharyngeal arches participating craniofacial development. mTOR deletion elicited a proliferation deficit and excessive apoptosis of post-migratory NCCs, leading to growth arrest of the facial primordia along with midline orofacial clefts. Furthermore, NCC differentiation was impaired. Thus, NCC derivatives, such as skeletons, vasculatures and neural tissues were either rudimentary or malformed. We further demonstrate that disruption of mTOR caused P53 hyperactivity and cell cycle arrest in cranial NCCs, and lowering P53 activity by one copy reduction attenuated the severity of craniofacial phenotype in NCC-mTOR knockout mice. Remarkably, NCC-Rptor disruption caused a spectrum of defects mirroring that of the NCC-mTOR deletion, whereas NCC-Rictor disruption only caused a mild craniofacial phenotype compared to the mTOR and Rptor conditional knockout models. Altogether, our data demonstrate that mTOR functions mediated by mTORC1 are indispensable for multiple processes of NCC development including proliferation, survival, and differentiation during craniofacial morphogenesis and organogenesis, and P53 hyperactivity in part accounts for the defective craniofacial development in NCC-mTOR knockout mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.