Tshz1 is required for axial skeleton, soft palate and middle ear development in mice
Tshz1 is required for axial skeleton, soft palate and middle ear development in mice
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DOI：
10.1016/j.ydbio.2007.05.038
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发表时间：
2007-08-15
影响因子：
2.7
通讯作者：
Fasano, Laurent
中科院分区：
文献类型：
--
作者：
Core, Nathalie;Caubit, Xavier;Fasano, Laurent
Tshz 基因家族的成员编码假定的锌指转录因子，这些转录因子在小鼠胚胎发生过程中广泛表达。 Tshz1 在体节、脊髓、肢芽和鳃弓中从 E9.5 中检测到。为了评估 Tshzl 在小鼠发育过程中的功能，我们生成了 Tslizl 缺陷小鼠。 Tshzl 失活会导致新生儿死亡并导致多种发育缺陷。在颅面区域，Tshzl 功能的丧失会导致中耳部件的特定畸形，包括锤骨和鼓室环。 Tvhzl(-/-)小鼠在颈部和胸部区域表现出Hox样椎骨畸形和同源异型转化，表明Tshzl和Hox基因参与控制骨骼形态发生的共同途径。最后，我们证明 Tshzl 是软腭发育所必需的。 (c) 2007 Elsevier Inc. 保留所有权利。
Members of the Tshz gene family encode putative zinc fingers transcription factors that are broadly expressed during mouse embryogenesis. Tshz1 is detected from E9.5 in the somites, the spinal cord, the limb buds and the branchial arches. In order to assess the function of Tshzl during mouse development, we generated Tslizl-deficient mice. Tshzl inactivation leads to neonatal lethality and causes multiple developmental defects. In the craniofacial region, loss of Tshzl function leads to specific malformations of middle ear components, including the malleus and the tympanic ring. Tvhzl(-/-) mice exhibited Hox-like vertebral malformations and homeotic transformations in the cervical and thoracic regions, suggesting that Tshzl and Hox genes are involved in common pathways to control skeletal morphogenesis. Finally, we demonstrate that Tshzl is required for the development of the soft palate. (c) 2007 Elsevier Inc. All rights reserved.