Tes regulates neural crest migration and axial elongation in Xenopus
Tes regulates neural crest migration and axial elongation in Xenopus
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DOI：
10.1016/j.ydbio.2006.02.004
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发表时间：
2006-05-01
影响因子：
2.7
通讯作者：
Smith, JC
中科院分区：
文献类型：
--
作者：
Dingwell, KS;Smith, JC
TES是一个新出现的蛋白质家族的成员，它共享一组被称为PET-LIM结构域的蛋白质基序。Pet-Lim蛋白，如棘刺，在非洲爪哇和斑马鱼的原肠形成过程中调节细胞行为，为了研究TES是否也参与控制细胞行为，我们分离了它的非洲爪哇同源基因。XTES被表达为母体转录本，一直维持在低水平，直到神经胚期，在头部和轴向结构中表达升高。XTES的耗尽会导致头部缩短和轴伸长的严重缺陷。前部的缺陷部分是由于抑制了脑神经脊部的迁移，而延伸性的缺陷可能是由于XFGF8、XDelta-1和Xcad-3的表达紊乱，从而扰乱了后半部的体格发育。最后，我们注意到同时耗尽XTES和非洲爪哇刺导致的轴向缺陷比单独耗尽XTES导致的轴向缺陷更严重，这表明这两种蛋白质共同作用控制轴向伸长。(C)2006 Elsevier Inc.保留所有权利。
Tes is a member of an emerging family of proteins sharing a set of protein motifs referred to as PET-LIM domains. PET-LIM proteins such as Prickle regulate cell behavior during gastrulation in Xenopus and zebrafish, and to ask whether Tes is also involved in controlling cell behavior, we isolated its Xenopus orthologue. Xtes is expressed as a maternal transcript that is maintained at low levels until neurula stages when expression is elevated in the head and axial structures. Depletion of Xtes leads to a foreshortened head and severe defects in axis elongation. The anterior defect is due in part to the inhibition of cranial neural crest migration while the defects in elongation may be due to perturbation of expression of XFGF8, Xdelta-1 and Xcad-3 and thereby to disruption of posterior somitogenesis. Finally, we note that simultaneous depletion of Xtes and Xenopus Prickle results in axial defects that are more severe than those resulting from depletion of Xtes alone, suggesting that the two proteins act together to control axial elongation. (c) 2006 Elsevier Inc. All rights reserved.