Specific craniofacial cartilage dysmorphogenesis coincides with a loss of dlx gene expression in retinoic acid-treated zebrafish embryos
Specific craniofacial cartilage dysmorphogenesis coincides with a loss of dlx gene expression in retinoic acid-treated zebrafish embryos
复制标题
DOI：
10.1016/s0925-4773(96)00616-8
复制
发表时间：
1997-01-01
影响因子：
2.6
通讯作者：
Ekker, M
中科院分区：
文献类型：
--
作者：
Ellies, DL;Langille, RM;Ekker, M
用维甲酸(RA)处理斑马鱼胚胎，一种已知会导致其他脊椎动物头面部软骨异常发育的物质，会导致胚胎几个区域的dir同源框基因表达的剂量和阶段依赖性损失。DIR在从后脑和内脏弓原基迁移的神经脊细胞中的表达对RA治疗特别敏感。当RA在顶细胞迁移之前或在顶细胞迁移期间使用时，观察到最强的影响，但如果在细胞进入弓部原基时使用RA，也可以观察到影响。Dir表达的缺失要么与源自后脑神经脊细胞的软骨成分缺失有关，要么与这些成分的形态异常有关。源自不表达dir基因的中脑神经脊细胞的软骨成分受到的影响较小。综上所述，在软骨凝聚之前内脏弓DIR表达的正常模式与即将分化的软骨元素的形态相似，我们的结果表明DIR基因是头面部软骨元素亚群发育的多步骤过程中的重要组成部分。(C)1997年爱思唯尔爱尔兰科学有限公司。
Treatments of zebrafish embryos with retinoic acid (RA), a substance known to cause abnormal craniofacial cartilage development in other vertebrates, result in dose- and stage-dependent losses of dir homeobox gene expression in several regions of the embryo. Dir expression in neural crest cells migrating from the hindbrain and in the visceral arch primordia is particularly sensitive to RA treatment. The strongest effects are observed when RA is administered prior to or during crest cell migration but effects can also be observed if RA is applied when the cells have entered the primordia of the arches. Losses of dir expression correlate either with the loss of cartilage elements originating from hindbrain neural crest cells or with abnormal morphology of these elements. Cartilage elements that originate from midbrain neural crest cells, which do not express dir genes, are less affected. Taken together with the observation that the normal patterns of visceral arch dir expression just prior to cartilage condensation resemble the morphology of the cartilage elements that are about to differentiate, our results suggest that dir genes are an important part of a multi-step process in the development of a subset of craniofacial cartilage elements. (C) 1997 Elsevier Science Ireland Ltd.