Literature DB >> 25511173

BCL11B expression in intramembranous osteogenesis during murine craniofacial suture development.

Greg Holmes1, Harm van Bakel2, Xueyan Zhou2, Bojan Losic2, Ethylin Wang Jabs2.   

Abstract

Sutures, where neighboring craniofacial bones are separated by undifferentiated mesenchyme, are major growth sites during craniofacial development. Pathologic fusion of bones within sutures occurs in a wide variety of craniosynostosis conditions and can result in dysmorphic craniofacial growth and secondary neurologic deficits. Our knowledge of the genes involved in suture formation is poor. Here we describe the novel expression pattern of the BCL11B transcription factor protein during murine embryonic craniofacial bone formation. We examined BCL11B protein expression at E14.5, E16.5, and E18.5 in 14 major craniofacial sutures of C57BL/6J mice. We found BCL11B expression to be associated with all intramembranous craniofacial bones examined. The most striking aspects of BCL11B expression were its high levels in suture mesenchyme and increasingly complementary expression with RUNX2 in differentiating osteoblasts during development. BCL11B was also expressed in mesenchyme at the non-sutural edges of intramembranous bones. No expression was seen in osteoblasts involved in endochondral ossification of the cartilaginous cranial base. BCL11B is expressed to potentially regulate the transition of mesenchymal differentiation and suture formation within craniofacial intramembranous bone.
Copyright © 2014 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Bone; Calvaria; Ctip2; Differentiation; Osteoblasts; Skull

Mesh:

Substances:

Year:  2014        PMID: 25511173      PMCID: PMC4369408          DOI: 10.1016/j.gep.2014.12.001

Source DB:  PubMed          Journal:  Gene Expr Patterns        ISSN: 1567-133X            Impact factor:   1.224


  43 in total

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8.  Cell mixing at a neural crest-mesoderm boundary and deficient ephrin-Eph signaling in the pathogenesis of craniosynostosis.

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9.  Evolution of a developmental mechanism: Species-specific regulation of the cell cycle and the timing of events during craniofacial osteogenesis.

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10.  Bcl11b transcription factor plays a role in the maintenance of the ameloblast-progenitors in mouse adult maxillary incisors.

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  6 in total

1.  BCL11B regulates sutural patency in the mouse craniofacial skeleton.

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2.  Multisystem Anomalies in Severe Combined Immunodeficiency with Mutant BCL11B.

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Journal:  N Engl J Med       Date:  2016-12-01       Impact factor: 91.245

Review 3.  Understanding craniosynostosis as a growth disorder.

Authors:  Kevin Flaherty; Nandini Singh; Joan T Richtsmeier
Journal:  Wiley Interdiscip Rev Dev Biol       Date:  2016-03-22       Impact factor: 5.814

4.  A de novo substitution in BCL11B leads to loss of interaction with transcriptional complexes and craniosynostosis.

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Journal:  Hum Mol Genet       Date:  2019-08-01       Impact factor: 6.150

Review 5.  Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.

Authors:  Marie-Thérèse Daher; Pedro Bausero; Onnik Agbulut; Zhenlin Li; Ara Parlakian
Journal:  Front Cell Dev Biol       Date:  2020-12-10

6.  The FaceBase Consortium: a comprehensive resource for craniofacial researchers.

Authors:  James F Brinkley; Shannon Fisher; Matthew P Harris; Greg Holmes; Joan E Hooper; Ethylin Wang Jabs; Kenneth L Jones; Carl Kesselman; Ophir D Klein; Richard L Maas; Mary L Marazita; Licia Selleri; Richard A Spritz; Harm van Bakel; Axel Visel; Trevor J Williams; Joanna Wysocka; Yang Chai
Journal:  Development       Date:  2016-06-10       Impact factor: 6.868

  6 in total

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