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源自潜在中胚层的信号对于斑马鱼神经嵴诱导而言并非必需。

Signals derived from the underlying mesoderm are dispensable for zebrafish neural crest induction.

作者信息

Ragland Jared W, Raible David W

机构信息

Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98195-7420, USA.

出版信息

Dev Biol. 2004 Dec 1;276(1):16-30. doi: 10.1016/j.ydbio.2004.08.017.

Abstract

Signals from the non-neural ectoderm, the neural ectoderm, and the underlying mesoderm have all been implicated in the induction of neural crest. Bone morphogenetic protein (BMP) signaling in particular has an important role in this process; however, it is unclear whether this activity of BMP is due to its effects on patterning the underlying mesoderm, to its ability to establish a competent neural plate boundary zone, or to the direct specification of neural crest at intermediate levels of activity within a BMP gradient. We show neural crest induction occurs in zebrafish in the absence of involuted mesoderm, indicating that this tissue and signals derived from it are dispensable for the formation of neural crest. Dorsal-involuted mesoderm is a major source of secreted BMP antagonists, and the activity of BMP signaling is thought to depend on the presence of the opposing activity of these antagonists. We find that the three BMP antagonists known to be expressed during gastrulation in zebrafish, noggin1, follistatin, and chordin, are dispensable for neural crest induction. These results suggest that mechanisms for restricting the spatio-temporal pattern of BMP expression may compensate for the loss of secreted BMP antagonist activity in establishing dorso-ventral patterning, neural induction, and the neural crest.

摘要

来自非神经外胚层、神经外胚层和下方中胚层的信号均与神经嵴的诱导有关。骨形态发生蛋白(BMP)信号传导在此过程中尤其起着重要作用;然而,尚不清楚BMP的这种活性是由于其对下方中胚层模式形成的影响,是由于其建立有能力的神经板边界区的能力,还是由于在BMP梯度内中等活性水平下对神经嵴的直接特化。我们发现,在没有内卷中胚层的情况下,斑马鱼中仍会发生神经嵴诱导,这表明该组织及其衍生的信号对于神经嵴的形成是可有可无的。背侧内卷中胚层是分泌型BMP拮抗剂的主要来源,并且BMP信号传导的活性被认为取决于这些拮抗剂的相反活性的存在。我们发现,已知在斑马鱼原肠胚形成过程中表达的三种BMP拮抗剂,即头蛋白1、卵泡抑素和脊索蛋白,对于神经嵴诱导是可有可无的。这些结果表明,限制BMP表达的时空模式的机制可能在建立背腹模式、神经诱导和神经嵴过程中补偿分泌型BMP拮抗剂活性的丧失。

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