The calcium pump of the endoplasmic reticulum plays a role in midline signaling during early zebrafish development

The calcium pump of the endoplasmic reticulum plays a role in midline signaling during early zebrafish development
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DOI:
10.1016/j.devbrainres.2004.03.016
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发表时间:
2004-07-19
期刊:
DEVELOPMENTAL BRAIN RESEARCH
影响因子:
--
通讯作者:
Creton, R
Creton, R
中科院分区:
其他
文献类型:
--
作者:
Creton, R

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在脊椎动物的早期发育过程中,沿着胚胎的中线激活了一个信号网络。这个信号网络感应神经管底板和大脑腹侧区域。反过来,腹侧脑区的诱导对于双侧前脑的分割和双眼的分离是重要的。本研究为内质网钙泵在斑马鱼中线信号转导中的作用提供了直接证据。在斑马鱼胚胎中,使用thapsigargin或clopiazonic酸可抑制内质网钙泵。在原肠形成早期抑制内质网钙泵导致睫状视,类似于独眼水母、斜视的缺陷。独眼针头和Silberblick突变胚胎。相反,在原肠中期抑制内质网钙泵不会导致睫状眼,但会导致尾部缺陷,类似于在无尾突变胚胎中观察到的缺陷。这项研究首次将thapsigargin和clopiazonic acid与睫状眼的诱导联系起来。此外,所获得的结果为钙离子在胚胎发育中的作用提供了新的信息,并可能导致对全前脑畸形的机制的新见解,全前脑畸形是人类发育中一种相对常见的大脑缺陷。(C)2004爱思唯尔B.V.保留所有权利。
During early vertebrate development, a signaling network is activated along the midline of the embryo. This signaling network induces the neural tube floor plate and ventral brain regions. In turn, induction of the ventral brain region is important for bilateral division of the forebrain and bilateral separation of the eyes. The present study provides direct evidence for a role of the endoplasmic reticulum Ca2+ pump in zebrafish midline signaling. The endoplasmic reticulum Ca2+ pump was inhibited in zebrafish embryos using thapsigargin or cyclopiazonic acid. Inhibition of the endoplasmic reticulum Ca2+ pump during early gastrulation induces cyclopia, mimicking defects observed in cyclops, squint.. one-eyed pinhead, and silberblick mutant embryos. In contrast, inhibition of the endoplasmic reticulum Ca2+ pump during mid-gastrulation does not induce cyclopia, but does induce tail defects, mimicking defects observed in no-tail mutant embryos. This study is the first to relate thapsigargin and cyclopiazonic acid with induction of cyclopia. In addition, obtained results provide new information on the roles of Ca2+ in embryonic development and may lead to new insights on the mechanisms underlying holoprosencephaly, a relatively common brain defect in human development. (C) 2004 Elsevier B.V. All rights reserved.