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Reduced O 2 and elevated ROS in sea urchin embryos leads to defects in ectoderm differentiation
Author(s) -
Agca Cavit,
Klein William H.,
Venuti Judith M.
Publication year - 2009
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22001
Subject(s) - ectoderm , biology , sea urchin , microbiology and biotechnology , nodal , nodal signaling , transcription factor , embryogenesis , anatomy , embryo , genetics , gene , gastrulation
The sea urchin oral‐aboral (OA) axis is established in part by Nodal signaling. The OA axis is also influenced by treatments affecting respiration and Nodal transcription is influenced by redox‐dependent transcription factors. This suggests that intracellular redox state plays a role in OA axis specification. Since cellular redox state can be altered by the formation of excess reactive oxygen species (ROS), and hypoxia and paraquat generate ROS in cells, we asked whether these treatments affected specification of the OA axis and Nodal expression. Embryos cultured under conditions that elevate ROS, demonstrate perturbed ectoderm specification, but other territories are not affected. Immunohistochemical and Q‐RT‐PCR analyses revealed that both oral and aboral ectoderm genes are downregulated. Our results argue that elevating ROS in sea urchin embryos by these treatments blocks early steps in ectoderm differentiation preceding the polarization of the ectoderm into oral and aboral territories. Developmental Dynamics 238:1777–1787, 2009. © 2009 Wiley‐Liss, Inc.