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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >BMP inhibition initiates neural induction via FGF signaling and Zic genes
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BMP inhibition initiates neural induction via FGF signaling and Zic genes

机译：BMP抑制通过FGF信号传导和Zic基因启动神经诱导

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摘要

Neural induction is the process that initiates nervous system development in vertebrates. Two distinct models have been put forward to describe this phenomenon in molecular terms. The default model states that ectoderm cells are fated to become neural in absence of instruction, and do so when bone morpho-genetic protein (BMP) signals are abolished. A more recent view implicates a conserved role for FGF signaling that collaborates with BMP inhibition to allow neural fate specification. Using the Xenopus embryo, we obtained evidence that may unite the 2 views. We show that a dominant-negative R-Smad, Smad5-somitabun-unlike the other BMP inhibitors used previously-can trigger conversion of Xenopus epidermis into neural tissue in vivo. However, it does so only if FGF activity is uncompromised. We report that this activity may be encoded by FGF4, as its expression is activated upon BMP inhibition, and its knockdown suppresses endogenous, as well as ectopic, neural induction by Smad5-somitabun. Supporting the importance of FGF instructive activity, we report the isolation of 2 immediate early neural targets, zic3 and foxD5a. Conversely, we found that zid can be activated by BMP inhibition in the absence of translation. Finally, Zic1 and Zic3 are required together for definitive neural fate acquisition, both in ectopic and endogenous situations. We propose to merge the previous models into a unique one whereby neural induction is controlled by BMP inhibition, which activates directly, and, via FGF instructive activity, early neural regulators such as Zic genes.
机译：神经诱导是启动脊椎动物神经系统发育的过程。提出了两种不同的分子模型来描述这种现象。默认模型指出，在没有指导的情况下，外胚层细胞注定会变成神经元，而当骨形态发生蛋白（BMP）信号被废除时，外胚层细胞会注定会变成神经元。最近的观点暗示了FGF信号转导的保守作用，其与BMP抑制协作以允许神经命运规范。使用非洲爪蟾胚胎，我们获得了可以使两种观点统一的证据。我们显示，与以前使用的其他BMP抑制剂不同，显性负性R-Smad，Smad5-索马他巴敦可以触发非洲爪蟾表皮向体内神经组织的转化。但是，只有在不损害FGF活性的情况下，才这样做。我们报道，这项活动可能是由FGF4编码，因为其表达在BMP抑制后被激活，其敲低抑制了Smad5-somitabun的内源性和异位神经诱导。支持FGF指导活动的重要性，我们报告了2个立即早期神经靶标zic3和foxD5a的分离。相反，我们发现zid可以在不存在翻译的情况下被BMP抑制激活。最后，在异位和内源情况下，需要Zic1和Zic3才能获得确定的神经命运。我们建议将先前的模型合并成一个独特的模型，从而通过BMP抑制来控制神经诱导，BMP抑制直接激活早期的神经调节剂，例如Zic基因，并通过FGF指导活性。

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    Leslie Marchal; Guillaume Luxardi; Virginie Thome; Laurent Kodjabachian;

  • 作者单位

    Institut de Biologie du Developpement de Marseille Luminy, UMR 6216, CNRS-Universite de la Mediterranee, 13288 Marseille Cedex 09, France;

    Institut de Biologie du Developpement de Marseille Luminy, UMR 6216, CNRS-Universite de la Mediterranee, 13288 Marseille Cedex 09, France;

    Institut de Biologie du Developpement de Marseille Luminy, UMR 6216, CNRS-Universite de la Mediterranee, 13288 Marseille Cedex 09, France;

    Institut de Biologie du Developpement de Marseille Luminy, UMR 6216, CNRS-Universite de la Mediterranee, 13288 Marseille Cedex 09, France;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    xenopus; default model; smad5-sbn;

    机译：爪蟾默认模型smad5-sbn;

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