All-trans retinoic acid-induced ectopic limb and caudal structures: murine strain sensitivities and pathogenesis.
All-trans retinoic acid-induced ectopic limb and caudal structures: murine strain sensitivities and pathogenesis.
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全反式视黄酸诱导的异位肢体和尾部结构：小鼠品系敏感性和发病机制。
DOI：
10.1002/dvdy.21568
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Collins,MichaelD
中科院分区：
文献类型：
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作者：
Liao,Xiaoyan;Collins,MichaelD
用维甲酸(RA)处理处于卵筒阶段的怀孕小鼠，已导致后代后肢异位。异位后肢的原因被认为包括同源转换或多轴形成。两个小鼠品系对这种畸形的易感性存在差异(C57BL/6N，高度敏感；SWV/FNN，不敏感)。异位肢体为后肢(表达Pitx1和Tbx4，但不表达Tbx5)，但也主要表达前肢Hoxb8。异位的原始条纹、脊索和结节的基因表达，以及对前内脏内胚层和中胚层迁移的抑制，表明异位体轴的形成。胚胎发育越早，异位后肢发育和轴形成的比率就越高。异位轴形成和细胞迁移抑制与畸形发生具有相同的应变易感性。我们认为，所有额外的后肢都来自异位轴的形成，其扰动是遗传背景相关的。发展动力学237：1553-1564,2008。©2008 Wiley-Liss，Inc.
Treatment of pregnant mice at the egg cylinder stage with retinoic acid (RA) has caused ectopic hindlimbs in the offspring. Proposed causes of ectopic hindlimbs include homeotic transformation or multiple axis formation. Two mouse strains were determined to be divergent in susceptibility to this malformation (C57BL/6N, highly sensitive; SWV/Fnn, less sensitive). Ectopic limbs were hindlimbs (expressingPitx1andTbx4but notTbx5), yet they also expressed the predominantly forelimbHoxb8. Ectopic body axis formation was indicated by gene expression for ectopic primitive streaks, notochords, and nodes, as well as inhibition of anterior visceral endoderm and mesodermal migration. The earlier in development that embryos were examined, the higher the rate of ectopic hindlimb development and axis formation. Ectopic axis formation and cell migration inhibition had the same strain susceptibility as the dysmorphogenesis. We propose that all extra hindlimbs were derived from ectopic axis formation, perturbation of which is genetic background dependent. Developmental Dynamics 237:1553–1564, 2008. © 2008 Wiley‐Liss, Inc.