Hensen's node from vitamin A-deficient quail embryo induces chick limb bud duplication and retains its normal asymmetric expression of Sonic hedgehog (Shh).

Hensen's node from vitamin A-deficient quail embryo induces chick limb bud duplication and retains its normal asymmetric expression of Sonic hedgehog (Shh).
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来自缺乏维生素 A 的鹌鹑胚胎的 Hensen 节诱导雏鸡肢芽复制,并保留其正常的 Sonic Hedgehog (Shh) 不对称表达。

DOI:
10.1006/dbio.1996.0021
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发表时间:
1996
期刊:
Developmental biology.
影响因子:
--
通讯作者:
Zile,MH
Zile,MH
中科院分区:
--
文献类型:
--
作者:
Chen,Y;Dong,D;Kostetskii,I;Zile,MH

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众所周知,鸡胚胎中的组织中心汉森结和外源性视黄酸在移植或应用于宿主鸡肢芽时都会诱导肢体复制。已知视黄酸存在于结节中,并被提议作为雏鸡肢体发育的假定形态发生素。在这里,我们报告来自维生素 A 缺乏的鹌鹑胚胎的 Hensen 结在宿主鸡胚胎中诱导肢体复制,类似于来自维生素 A 充足的对照胚胎的结所诱导的肢体复制。我们还证明,最近被证明是鸡肢芽中极化活性介导物的 Sonic Hedgehog (Shh) 的表达不受胚胎内源维生素 A 状态的影响。此外,整体原位杂交揭示了维生素A充足和缺乏的鹌鹑胚胎的Hensen节中Shh表达的不对称性。在获得缺乏维生素A的胚胎的鸡蛋中未检测到类维生素A。正常胚胎的提取物诱导的报告基因表达水平相当于每个胚胎中存在 3.4 pg 活性类维生素A,而维生素 A 缺乏胚胎的提取物诱导的报告基因表达基线水平与对照相似。我们的研究表明,内源性视黄酸不参与Shh表达,也不参与正常早期禽类胚胎发生过程中其不对称性的调节,并支持当前的观点,即内源性视黄酸可能不是肢芽复制的直接形态发生素。
Both Hensen's node, the organizer center in chick embryo, and exogenous retinoic acid are known to induce limb duplication when grafted or applied to the host chick limb bud. Retinoic acid is known to be present in the node and has been proposed as the putative morphogen for chick limb development. Here, we report that Hensen's node from vitamin A-deficient quail embryo induces limb duplication in the host chick embryo similar to that induced by the node from vitamin A-sufficient control embryos. We also demonstrate that the expression ofSonic hedgehog(Shh), recently shown to be the mediator of polarizing activity in the chick limb bud, is not affected by the endogenous vitamin A status of the embryo. Furthermore, whole-mountin situhybridization revealed asymmetry ofShhexpression in the Hensen's node of both vitamin A-sufficient and -deficient quail embryos. Retinoids were not detectable in the eggs from which vitamin A-deficient embryos were obtained. Extracts from normal embryos induced a level of expression of reporter gene equivalent to the presence of 3.4 pg of active retinoids per embryo, while those from vitamin A-deficient embryos induced a baseline level of reporter gene expression similar to that of the controls. Our studies suggest that endogenous retinoic acid is not involved inShhexpression nor in regulating its asymmetry during normal early avian embryogenesis and support the current view that endogenous retinoic acid may not be a direct morphogen for limb bud duplication.
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