Stage-dependent craniofacial defects resulting from Sprouty2 overexpression
Stage-dependent craniofacial defects resulting from Sprouty2 overexpression
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DOI：
10.1002/dvdy.21195
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发表时间：
2007-07-01
影响因子：
2.5
通讯作者：
Helms, Jill A.
中科院分区：
文献类型：
--
作者：
Goodnough, L. Henry;Brugmann, Samantha A.;Helms, Jill A.
发芽基因编码在多种发育事件中起作用的受体酪氨酸激酶的细胞内调节因子。尽管携带斯普罗蒂基因零突变的小鼠表现出颅面异常，但这些调节蛋白在面部发育中的确切作用仍不清楚。在这里，我们发现在颅面发育开始时过度表达spry2会导致面部突出部生长的急剧停滞。虽然内源性spry2和成纤维细胞生长因子8 （fgf8）在颅面发育的大部分过程中共表达，但spry2的过表达并未改变fgf靶基因表达的时空模式。spry2过表达的形态学后果是特异性的：所有的面部突出部分都被截断，但尽管有这种明显的畸形，但骨形成和软骨形成的程序并未受损。总的来说，这些数据表明Sprouty2在面部突出的生长中起着独立于典型Fgf信号的作用。科学进展(6):1818 - 1828,2007。(c) 2007 Wiley-Liss, Inc。
Sprouty genes encode intracellular regulators of receptor tyrosine kinases that function in a variety of developmental events. Although mice carrying null mutations in Sprouty genes exhibit craniofacial anomalies, the precise role of these regulatory proteins in facial development remains unclear. Here, we show that overexpression of spry2 at the initiation of craniofacial development results in a dramatic arrest in outgrowth of the facial prominences. Although endogenous spry2 and fibroblast growth factor 8 (fgf8) are coexpressed throughout much of craniofacial development, overexpression of spry2 did not alter the spatiotemporal patterns of fgf target gene expression. The morphological consequences of spry2 overexpression were specific: all of the facial prominences were truncated, but despite this gross malformation, the programs of osteogenesis and chondrogenesis were not impaired. Collectively, these data suggest that Sprouty2 plays a role in the outgrowth of facial prominences independent of canonical Fgf signaling. Developmental Dynamics 236:1918-1928, 2007. (c) 2007 Wiley-Liss, Inc.