Tags

Type your tag names separated by a space and hit enter

BCL11B regulates sutural patency in the mouse craniofacial skeleton.
Dev Biol 2016; 415(2):251-260DB

Abstract

The transcription factor BCL11B plays essential roles during development of the immune, nervous, and cutaneous systems. Here we show that BCL11B is expressed in both osteogenic and sutural mesenchyme of the developing craniofacial complex. Bcl11b(-/-) mice exhibit increased proliferation of osteoprogenitors, premature osteoblast differentiation, and enhanced skull mineralization leading to synostoses of facial and calvarial sutures. Ectopic expression of Fgfr2c, a gene implicated in craniosynostosis in mice and humans, and that of Runx2 was detected within the affected sutures of Bcl11b(-/-) mice. These data suggest that ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice.

Authors+Show Affiliations

Department of Pharmaceutical Sciences, College of Pharmacy, USA.Skeletal Biology Laboratory, School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR 97331, USA.Department of Pharmaceutical Sciences, College of Pharmacy, USA.Department of Pharmaceutical Sciences, College of Pharmacy, USA; Department of Integrative Biosciences, Oregon Health & Science University, Portland, OR 97201, USA. Electronic address: mark.leid@oregonstate.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

26453795

Citation

Kyrylkova, Kateryna, et al. "BCL11B Regulates Sutural Patency in the Mouse Craniofacial Skeleton." Developmental Biology, vol. 415, no. 2, 2016, pp. 251-260.
Kyrylkova K, Iwaniec UT, Philbrick KA, et al. BCL11B regulates sutural patency in the mouse craniofacial skeleton. Dev Biol. 2016;415(2):251-260.
Kyrylkova, K., Iwaniec, U. T., Philbrick, K. A., & Leid, M. (2016). BCL11B regulates sutural patency in the mouse craniofacial skeleton. Developmental Biology, 415(2), pp. 251-260. doi:10.1016/j.ydbio.2015.10.010.
Kyrylkova K, et al. BCL11B Regulates Sutural Patency in the Mouse Craniofacial Skeleton. Dev Biol. 2016 07 15;415(2):251-260. PubMed PMID: 26453795.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - BCL11B regulates sutural patency in the mouse craniofacial skeleton. AU - Kyrylkova,Kateryna, AU - Iwaniec,Urszula T, AU - Philbrick,Kenneth A, AU - Leid,Mark, Y1 - 2015/10/09/ PY - 2015/07/01/received PY - 2015/09/19/revised PY - 2015/10/06/accepted PY - 2015/10/11/entrez PY - 2015/10/11/pubmed PY - 2017/6/27/medline KW - BCL11B/CTIP2 KW - Craniofacial development KW - Craniosynostosis KW - Fgfr2c KW - Midfacial hypoplasia KW - Runx2 KW - Twist1 SP - 251 EP - 260 JF - Developmental biology JO - Dev. Biol. VL - 415 IS - 2 N2 - The transcription factor BCL11B plays essential roles during development of the immune, nervous, and cutaneous systems. Here we show that BCL11B is expressed in both osteogenic and sutural mesenchyme of the developing craniofacial complex. Bcl11b(-/-) mice exhibit increased proliferation of osteoprogenitors, premature osteoblast differentiation, and enhanced skull mineralization leading to synostoses of facial and calvarial sutures. Ectopic expression of Fgfr2c, a gene implicated in craniosynostosis in mice and humans, and that of Runx2 was detected within the affected sutures of Bcl11b(-/-) mice. These data suggest that ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice. SN - 1095-564X UR - https://www.unboundmedicine.com/medline/citation/26453795/BCL11B_regulates_sutural_patency_in_the_mouse_craniofacial_skeleton_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0012-1606(15)30228-1 DB - PRIME DP - Unbound Medicine ER -