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关注:1 2013-05-23 12:21

求翻译:During the early stages of body axis extension, retinoic acid (RA) synthesized in somites by Raldh2 represses caudal FGF signaling to limit the tailbud progenitor zone. Excessive RA down-regulates Fgf8 and triggers premature termination of body axis extension, suggesting that endogenous RA may function in normal termination of body axis extension. Here, we demonstrate that Raldh2-/- mouse embryos undergo normal down-regulation of tailbud Fgf8 expression and termination of body axis extension. Interestingly, Raldh2 expression in tail somites and tailbud from E10.5 onwards does not result in RA activity monitored by RARE-lacZ. Treatment of tailbuds with physiological levels of RA or retinaldehyde induces RARE-lacZ activity, validating the sensitivity of RARE-lacZ and demonstrating deficient RA synthesis in tail somites and tailbud due to a lack of retinaldehyde synthesis. These studies demonstrate an early uncoupling of RA signaling from mouse tailbud development and show that termination of body axis extension occurs in the absence of RA signaling. 是什么意思?

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During the early stages of body axis extension, retinoic acid (RA) synthesized in somites by Raldh2 represses caudal FGF signaling to limit the tailbud progenitor zone. Excessive RA down-regulates Fgf8 and triggers premature termination of body axis extension, suggesting that endogenous RA may function in normal termination of body axis extension. Here, we demonstrate that Raldh2-/- mouse embryos undergo normal down-regulation of tailbud Fgf8 expression and termination of body axis extension. Interestingly, Raldh2 expression in tail somites and tailbud from E10.5 onwards does not result in RA activity monitored by RARE-lacZ. Treatment of tailbuds with physiological levels of RA or retinaldehyde induces RARE-lacZ activity, validating the sensitivity of RARE-lacZ and demonstrating deficient RA synthesis in tail somites and tailbud due to a lack of retinaldehyde synthesis. These studies demonstrate an early uncoupling of RA signaling from mouse tailbud development and show that termination of body axis extension occurs in the absence of RA signaling.
问题补充:

  • 匿名
2013-05-23 12:26:38
体轴扩展的早期阶段,视黄酸 (RA) Raldh2 somites 的合成压抑骶管 FGF 限制 tailbud 祖带信号。过度 RA 下调 Fgf8 和触发体轴扩展,提前终止建议内源性 RA 可能函数体轴延长正常终止。在这里,我们证明 Raldh2/小鼠胚胎接受 tailbud Fgf8 表达的正常下调节和体轴延长终止。有趣的是,尾 somites 及 tailbud E10.5 从起 Raldh2 表达不会导致受稀土 lacZ RA 活动。生理水平的 RA 或 retinaldehyde tailbuds 治疗诱导稀土 lacZ 活动,验证的稀土 lacZ 敏感性和演示缺角合成的尾 somites 和 tailbud 的 retinaldehyde 合成的缺乏。这些研究表明早期耦的 RA 信号从鼠标 tailbud 发展和放映中的 RA 信号没有发生体轴延长终止。
 
 
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