ArticleAmerican journal of medical genetics. Part A2013
Postnatal brain and skull growth in an Apert syndrome mouse model.
Article in American journal of medical genetics. Part A, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Distinct disease mutations in DNMT3A result in a spectrum of behavioral, epigenetic, and transcriptional deficits.Cell reports · 2023Article
- Evolution, conservatism and overlooked homologies of the mammalian skull.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Synchondrosis fusion contributes to the progression of postnatal craniofacial dysmorphology in syndromic craniosynostosis.Journal of anatomy · 2023Article
- Distinct disease mutations in DNMT3A result in a spectrum of behavioral, epigenetic, and transcriptional deficits.bioRxiv : the preprint server for biology · 2023Article
- Morphological correspondence between brain and endocranial surfaces in mice exposed to undernutrition during development.Journal of anatomy · 2022Article
- DNMT3A Haploinsufficiency Results in Behavioral Deficits and Global Epigenomic Dysregulation Shared across Neurodevelopmental Disorders.Cell reports · 2020Article
- ViceCT and whiceCT for simultaneous high-resolution visualization of craniofacial, brain and ventricular anatomy from micro-computed tomography.Scientific reports · 2020Article
- Aberrant cell segregation in the craniofacial primordium and the emergence of facial dysmorphology in craniofrontonasal syndrome.PLoS genetics · 2020Article
- Quantification of gene expression patterns to reveal the origins of abnormal morphogenesis.eLife · 2018Article
- Body size and allometric variation in facial shape in children.American journal of physical anthropology · 2018Article
- Deformed Skull Morphology Is Caused by the Combined Effects of the Maldevelopment of Calvarias, Cranial Base and Brain in FGFR2-P253R Mice Mimicking Human Apert Syndrome.International journal of biological sciences · 2017Article
- Two Hundred Thirty-Six Children With Developmental Hydrocephalus: Causes and Clinical Consequences.Journal of child neurology · 2016Article
- Performance of single and multi-atlas based automated landmarking methods compared to expert annotations in volumetric microCT datasets of mouse mandibles.Frontiers in zoology · 2015Article
- Morphometrics, 3D Imaging, and Craniofacial Development.Current topics in developmental biology · 2015Review
- Closing the Gap: Genetic and Genomic Continuum from Syndromic to Nonsyndromic Craniosynostoses.Current genetic medicine reports · 2014Article
- Infantile hydrocephalus: a review of epidemiology, classification and causes.European journal of medical genetics · 2014Review
- Embryonic craniofacial bone volume and bone mineral density in Fgfr2(+/P253R) and nonmutant mice.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Craniofacial divergence by distinct prenatal growth patterns in Fgfr2 mutant mice.BMC developmental biology · 2014Article
- Hand in glove: brain and skull in development and dysmorphogenesis.Acta neuropathologica · 2013Review
- Tissue-specific responses to aberrant FGF signaling in complex head phenotypes.Developmental dynamics : an official publication of the American Association of Anatomists · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Craniofacial and neural tissues develop in concert throughout prenatal and postnatal growth. FGFR-related craniosynostosis syndromes, such as Apert syndrome (AS), are associated with specific phenotypes involving both the skull and the brain. We analyzed the effects of the FGFR P253R mutation for AS using the Fgfr2(+/P253R) Apert syndrome mouse to evaluate the effects of this mutation on these two tissues over the course of development from day of birth (P0) to postnatal day 2 (P2). Three-dimensional magnetic resonance microscopy and computed tomography images were acquired from Fgfr2(+/P253R) mice and unaffected littermates at P0 (N = 28) and P2 (N = 20).Three-dimensional coordinate data for 23 skull and 15 brain landmarks were statistically compared between groups. Results demonstrate that the Fgfr2(+/P253R) mice show reduced growth in the facial skeleton and the cerebrum, while the height and width of the neurocranium and caudal regions of the brain show increased growth relative to unaffected littermates. This localized correspondence of differential growth patterns in skull and brain point to their continued interaction through development and suggest that both tissues display divergent postnatal growth patterns relative to unaffected littermates. However, the change in the skull-brain relationship from P0 to P2 implies that each tissue affected by the mutation retains a degree of independence, rather than one tissue directing the development of the other.
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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.