The medaka zic1/zic4 mutant provides molecular insights into teleost caudal fin evolution.

The medaka zic1/zic4 mutant provides molecular insights into teleost caudal fin evolution.
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青鳉 zic1/zic4 突变体为硬骨鱼尾鳍进化提供了分子视角。

DOI:
10.1016/j.cub.2012.01.063
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发表时间:
2012
期刊:
影响因子:
9.2
通讯作者:
Yuuta Moriyama
Yuuta Moriyama
中科院分区:
生物学1区
文献类型:
--
作者:
岡部正隆;佐藤正純;原口徳子;Yuuta Moriyama

文献摘要

相似文献

硬骨鱼有一个不对称的尾鳍骨架,由身体轴的最尾部向上弯曲形成,乌拉尔地区[1-3]。这种同尾型的尾鳍确保了强大而复杂的运动,被认为是硬骨鱼类在水生环境中适应辐射过程中最重要的创新之一[4-6]。然而,造成不对称尾鳍的机制在很大程度上仍然未知。自发的青鳉(硬骨鱼)突变体,双臀鳍(Da),具有独特的对称尾部骨骼,类似于在Polypterus和腔棘鱼中看到的双尾型。我们对Damutant进行了详细的分析,以获得对尾鳍形态发生的分子见解。我们首先证明,一个大的转座子,插入到增强子区的zic 1和zic 4基因(zic 1/zic 4)在Da,是与中胚层特异性的转录损失。然后,我们表明,zic 1/zic 4强烈表达在背部的乌拉尔间充质,从而诱导不对称尾鳍发育在野生型胚胎,而他们的表达是失去了在Da。比较分析进一步表明zic 1/zic 4在硬骨鱼中的背中胚层表达是保守的,突出了zic 1/zic 4在尾鳍形态发生中的关键作用。
Teleosts have an asymmetrical caudal fin skeleton formed by the upward bending of the caudal-most portion of the body axis, the ural region [1–3]. This homocercal type of caudal fin ensures powerful and complex locomotion and is regarded as one of the most important innovations for teleosts during adaptive radiation in an aquatic environment [4–6]. However, the mechanisms that create asymmetric caudal fin remain largely unknown. The spontaneous medaka (teleost fish) mutant,Double anal fin(Da), exhibits a unique symmetrical caudal skeleton that resembles the diphycercal type seen inPolypterusand Coelacanth. We performed a detailed analysis of theDamutant to obtain molecular insight into caudal fin morphogenesis. We first demonstrate that a large transposon, inserted into the enhancer region of thezic1andzic4genes (zic1/zic4) inDa, is associated with the mesoderm-specific loss of their transcription. We then show thatzic1/zic4are strongly expressed in the dorsal part of the ural mesenchyme and thereby induce asymmetric caudal fin development in wild-type embryos, whereas their expression is lost inDa. Comparative analysis further indicates that the dorsal mesoderm expression ofzic1/zic4is conserved in teleosts, highlighting the crucial role ofzic1/zic4in caudal fin morphogenesis.