Respecification of ectoderm and altered Nodal expression in sea urchin embryos after cobalt and nickel treatment

被引:13
作者
Agca, Cavit [1 ]
Klein, William H. [2 ]
Venuti, Judith M. [1 ]
机构
[1] Louisiana State Univ, Hlth Sci Ctr, Dept Cell Biol & Anat, New Orleans, LA 70112 USA
[2] Univ Texas MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA
关键词
Cobalt; Nickel; Nodal signaling; Oral ectoderm; Ectoderm; Oralization; ECHINODERM BILATERAL DETERMINATION; ORAL-ABORAL AXIS; LEFT-RIGHT ASYMMETRY; TRANSCRIPTION FACTOR; GROWTH-FACTOR; P38; MAPK; SPECIFICATION; GENES; INHIBITION; PROTEIN;
D O I
10.1016/j.mod.2009.01.005
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In the sea urchin embryo, Nodal is the earliest known signal to play a role in the specification of the oral ectodermal territory. Nodal, a TGF-beta ligand, is first expressed in the presumptive oral ectoderm at similar to 7 H of development. Nodal overexpression produces a distinctive bell-shaped phenotype with expanded oral ectoderm, which resembles the oralized phenotype obtained as a result of nickel (Ni) treatment. To date, a detailed analysis of gene expression in Ni-treated embryos has not been undertaken. Because treatment with cobalt (Co) produces similar results to those seen with Ni treatment in other systems, we were interested in determining how Co influences sea urchin embryonic development. Here we report that Co also induces oralization of the ectoderm, and the effects of Ni and Co depend on functional Nodal signaling. Although both metals upregulate nodal gene expression, they do not initiate nodal transcription precociously Analysis of the perturbation of Nodal receptor function suggests that Ni and Co contribute to nodal upregulation in the absence of nodal autoregulation, but cannot fully oralize the ectoderm. in the absence of Nodal signaling. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:430 / 442
页数:13
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