Premium
Analysis of the effects of nickel, cobalt and ROS on Nodal signaling and axis specification in sea urchin embryos
Author(s) -
Venuti Judith M.,
Agca Cavit,
Klein William H.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.473.6
Subject(s) - ectoderm , nodal signaling , sea urchin , nodal , microbiology and biotechnology , downregulation and upregulation , biology , embryogenesis , transcription factor , embryo , chemistry , anatomy , biochemistry , gastrulation , gene
Nodal is asymmetrically expressed in the early sea urchin embryo and is the earliest indicator of the oral ectoderm territory. Nickel (Ni) treatment oralizes ectoderm and expands nodal expression, but the mechanism of Ni's action is unclear. In other systems, Ni generates reactive oxygen species (ROS) and stabilizes hypoxia inducible factors (HIFs). Since Cobalt (Co) has similar effects to Ni, we were interested in determining if Co similarly influenced sea urchin development. We show that, Co, like Ni oralizes ectoderm and upregulates nodal expression. Although neither metal induces nodal transcription precociously, both upregulate nodal expression after its initial activation. Because redox signaling is thought to be an important component of axis specification in sea urchin embryos we investigated the consequences of elevating ROS by other means. Both hypoxia and paraquat elevate ROS in vertebrate cells. However, hypoxia and paraquat treatment do not oralize sea urchin embryos or upregulate nodal significantly; instead, ectoderm specification is repressed while specification of other lineages is unaffected. Furthermore, an analysis of sea urchin HIFs suggests that Co and Ni are unlikely to influence ectoderm specification through the HIF pathway. Supported by the LSUHSC Enhancement Fund (JMV) and the Robert A.Welch Foundation (WHK).