ArticleDevelopmental biology2016
MEMO1 drives cranial endochondral ossification and palatogenesis.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway.Development (Cambridge, England) · 2024Article
- MEMO1 Is Required for Ameloblast Maturation and Functional Enamel Formation.Journal of dental research · 2023Article
- FGFR regulator Memo1 is dispensable for FGF23 expression by osteoblasts during folic acid-driven kidney injury.Physiological reports · 2023Article
- Knockdown of circRNA-Memo1 Reduces Hypoxia/Reoxygenation Injury in Human Brain Endothelial Cells Through miRNA-17-5p/SOS1 Axis.Molecular neurobiology · 2022Article
- Article
- The Mafb cleft-associated variant H131Q is not required for palatogenesis in the mouse.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Review
- Redox-Dependent Bone Alkaline Phosphatase Dysfunction Drives Part of the Complex Bone Phenotype in Mice Deficient forJBMR plus · 2018Article
- Article
- Face morphogenesis is promoted by Pbx-dependent EMT via regulation ofDevelopment (Cambridge, England) · 2018Article
- AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning.Development (Cambridge, England) · 2018Article
- TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF.PLoS genetics · 2017Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The cranial base is a component of the neurocranium and has a central role in the structural integration of the face, brain and vertebral column. Consequently, alteration in the shape of the human cranial base has been intimately linked with primate evolution and defective development is associated with numerous human facial abnormalities. Here we describe a novel recessive mutant mouse strain that presented with a domed head and fully penetrant cleft secondary palate coupled with defects in the formation of the underlying cranial base. Mapping and non-complementation studies revealed a specific mutation in Memo1 - a gene originally associated with cell migration. Expression analysis of Memo1 identified robust expression in the perichondrium and periosteum of the developing cranial base, but only modest expression in the palatal shelves. Fittingly, although the palatal shelves failed to elevate in Memo1 mutants, expression changes were modest within the shelves themselves. In contrast, the cranial base, which forms via endochondral ossification had major reductions in the expression of genes responsible for bone formation, notably matrix metalloproteinases and markers of the osteoblast lineage, mirrored by an increase in markers of cartilage and extracellular matrix development. Concomitant with these changes, mutant cranial bases showed an increased zone of hypertrophic chondrocytes accompanied by a reduction in both vascular invasion and mineralization. Finally, neural crest cell-specific deletion of Memo1 caused a failure of anterior cranial base ossification indicating a cell autonomous role for MEMO1 in the development of these neural crest cell derived structures. However, palate formation was largely normal in these conditional mutants, suggesting a non-autonomous role for MEMO1 in palatal closure. Overall, these findings assign a new function to MEMO1 in driving endochondral ossification in the cranium, and also link abnormal development of the cranial base with more widespread effects on craniofacial shape relevant to human craniofacial dysmorphology.
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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.