Twist1 homodimers enhance FGF responsiveness of the cranial sutures and promote suture closure

被引:109
|
作者
Connerney, Jeannette [1 ,2 ]
Andreeva, Viktoria [1 ]
Leshem, Yael [1 ]
Mercado, Miguel A. [1 ]
Dowell, Karen [1 ]
Yang, Xuehei [1 ]
Lindner, Volkhard [1 ,2 ]
Friesel, Robert E. [1 ,2 ]
Spicer, Douglas B. [1 ,2 ]
机构
[1] Maine Med Ctr, Res Inst, Ctr Mol Med, Scarborough, ME 04074 USA
[2] Univ Maine, Dept Biochem Microbiol & Mol Biol, Orono, ME 04469 USA
关键词
Twist1; FGFR2; FGF; BMP; bHLH; craniosynostosis; calvaria; sutures; craniofacial; osteoblast differentiation;
D O I
10.1016/j.ydbio.2008.03.037
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Haploinsufficiency of the transcription factor TWIST1 is associated with Saethre-Chotzen Syndrome and is manifested by craniosynostosis, which is the premature closure of the calvaria sutures. Previously, we found that Twist1 forms functional homodimers and heterodimers that have opposing activities. Our data supported a model that within the calvaria sutures Twist1 homodimers (T/T) reside in the osteogenic fronts while Twist1/E protein heterodimers (T/E) are in the mid-sutures. Twist1 haploinsufficiency alters the balance between these dimers, favoring an increase in homodimer formation throughout the sutures. The data we present here further supports this model and extends it to integrate the Twist1 dimers with the pathways that are known to regulate cranial suture patency. This data provides the first evidence of a functional link between Twist1 and the FGF pathway, and indicates that differential regulation of FGF signaling by T/T and T/E dimers plays a central role in governing cranial suture patency. Furthermore, we show that inhibition of FGF signaling prevents craniosynostosis in Twist1(+/-) mice, demonstrating that inhibition of a signaling pathway that is not part of the initiating mutation can prevent suture fusion in a relevant genetic model of craniosynostosis. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:323 / 334
页数:12
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